T<H30I  B89Z 

CoUcgc  of  ^i)j>s!iciang  anlr  burgeons 


G.f-t  o/^ 


Dr.  C.F.  M^.cdoYxdd 


A  TEXT-BOOK 


DENTAL  PATHOLOGY 

AND 

THERAPEUTICS 


FOR  STUDENTS  AND  PRACTITIONERS 


BASED    UPON   THE    OEIGINAL    OF 


HENRY  H.  BURCHARD,  M.D.,  D.D.S. 

LATE  SPECIAL  LECTURER  ON  DENTAL  PATHOLOGY  AND  THERAPEUTICS  IN  THE  PHILADELPHIA 

DENTAL  COLLEGE 


REWRITTEN   BY 

OTTO  E.  INGLIS,  D.D.S. 

PROFESSOR   OF  DENTAL  PATHOLOGY  AND  THERAPEUTICS  IN  THE   PHILADELPHIA 
DENTAL   COLLEGE 


FIFTH  EDITION,  THOROUGHLY  REVISED 


ILLUSTRATED  WITH    708    ENGRAVINGS  AND   A   COLORED   PLATE 


LEA    &    FEBIGER 

PHILADELPHIA   AND   NEW   YORK 
1915 


30 
X 


1^(S- 


Entered  according  to  the  Act  of  Congress,  in  the  year  1915,  by 

LEA   &    FEBIGER, 
in  the  Of&ce  of  the  Librarian  of  Congress.     All  rights  reserved. 


THIS 

y  C'  L  r  ^i  E 

LS    EZSPECTrnXY    DEDICATED 
TO 

RUSSELL  H,  COXT\TLL,  D.D.,  LL.D. 

LN"    EECOGXTTIC'X    OF    HIS    rXSELTISH 

EFTOET?    EN"    THE 

OPEXEN'G    OF    CTPOEirXITEES 

FOE    EDrCATIOX. 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/textbookofdental1915burc 


PREFACE  TO  FIFTH  EDITIOAl 


This  volume  was  originally  designed  as  a  text-book  of  the  principles 
and  practice  of  dental  medicine  for  the  use  of  students,  and  as  a 
reference  work  on  applied  special  pathology  and  therapeutics  for 
the  use  of  dentists.  Accepting  the  dictum  of  the  advanced  teachers 
of  the  day,  it  was  considered  that  an  entirely  rational  system  of 
dental  medicine  could  have  but  one  basis — namely,  the  same  prin- 
ciples which  underlie  general  medical  and  surgical  practice.  The 
book  represents,  therefore,  an  attempt  at  formulating,  from  data 
obtained  from  every  available  source,  a  system  of  dental  pathology 
and  therapeutics  of  which  the  several  parts  shall  be  in  harmony  with 
one  another  and  also  with  the  several  collateral  sciences  involved. 
The  impulse  prompting  the  work  was  no  desire  to  multiply  books, 
but  arose  from  a  conviction  expressed  by  many  teachers,  that  such 
a  volume  was  needed  by  students,  practitioners,  and  teachers. 

In  revising  the  work  for  this  new  edition,  the  Editor  has  endeavored 
to  maintain  the  original  idea  of  a  text-book  furnishing  a  description 
of  each  dental  disease  and  its  treatment  in  such  manner  that  teachers 
may  find  it  a  useful  adjunct  in  the  presentation  of  dental  pathology 
and  therapeutics  to  their  students.  The  development  in  this  branch 
of  dental  science  during  the  last  few  years  has  necessitated  many 
changes  in  the  text  to  reflect  the  present  advanced  position  of  the 
entire  subject.  Many  new  illustrations  have  been  added  to  increase 
its  value  for  didactic  purposes. 

In  place  of  the  original  section  on  Pharmacology,  which  was 
necessarily  limited  in  scope,  the  various  remedies  and  drugs  men- 
tioned are  fully  indexed  in  order  that  their  various  uses  as  applied 
to  tlie  therapy  of  the  pathological  conditions  discussed  may  be  studied . 

The  thanks  of  the  Editor  are  due  to  those  who  have  kindly  loaned 
valuable  illustrations.    In  no  instance  has  a  request  been  denied. 

The  Editor  also  takes  this  opportunity  to  express  his  warm  appre- 
ciation of  the  continued  favor  bestowed  on  this  work  by  professors 
and  teachers  of  the  subject  throughout  this  Continent  and  in  Europe. 

O.  E.  Inglis. 

1524  Chestnut  Street, 
Philadelphia,  1915. 


CONTENTS. 

SECTION    I. 
GENERAL   PATHOLOGY. 

CHAPTER   I. 
General  Principles 17 

CHAPTER  II. 

Causes  of  Disease,  General  and  Local 28 

CHAPTER   III. 

Microorganisms  as  Exciting  Causes  of  Disease 36 

CHAPTER   IV. 
Disturbances  of  Nutrition 66 

CHAPTER  V. 

Disturbances  op  the  Vascular  System 113 


SECTION    I L 
EMBRYOLOGY,  ANATOMY,  AND  HISTOLOGY^ 

CHAPTER  VI. 

The  Development,  Anatomy  and  Histology  of  the  Jaws  and  Teeth  153 

CHAPTER  VII. 

Dentition:    Its  Progress,  Variations,  and  Attendant  Disorders  194 

CHAPTER  VIII. 
Malformations  and  Malpositions  of  the  Teeth 239 


viii  CONTENTS 

SECTIONIII. 
AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN. 

CHAPTER   IX, 
Abrasion,  Erosion,  and  Mechanical  Injury 299 

CHAPTER  X. 

Stains  of  the  Enamel  and  Dentin 329 

CHAPTER  XI. 

Dental  Caries:  History;  Exciting  and  Predisposing  Causes       .  337 

CHAPTER  XII. 

Dental  Caries:  Pathology,  Morbid  Anatomy,  and  Clinical  History     362 

CHAPTER  XIII. 

Dental  Caries:  Diagnosis,  Symptoms,  and  Prognosis 390 

CHAPTER  XIV. 

Dental  Caries:  Therapeutics  and  Prophylaxis s.     416 


SECTION    IV. 
DISEASES  OF  THE  DENTAL  PULP. 

CHAPTER  XV. 

Constructive  Diseases 447 

CHAPTER  XVI. 

Destructive  Diseases  of  the  Dental  Pulp 468 

CHAPTER  XVII. 

Methods  of  Removal  of  the  Dental  Pulp  and  Root-canal  Filling     515 

CHAPTER  XVIII. 

Gangrene  of -the  Pulp 562 


CONTENTS  ix 

SECTION    V. 
DISEASES  OF  THE  PERICEMENTUM. 

CHAPTER  XIX. 

Septic  Apical  Pericementitis  (AcuteX 585 

CHAPTER   XX. 

Chronic  Septic,   Purulent,  Apical  Pericementitis   (Chronic  Apical 

Abscess) 609 

CHAPTER  XXI. 
Non-septic  Pericementitis 644 


SECTION    VI. 

PERICEMENTAL  DISEASES  BEGINNING  AT  THE 
GUM  MARGIN. 

CHAPTER  XXII. 
Gingivitis 673 

CHAPTER  XXIII. 

Salivary  and  Serumal  Calculus 692 

CHAPTER  XXIV. 
Pyorrhea  Alveolaris 713 

CHAPTER  XXV. 
Pericemental  Abscess 745 

CHAPTER  XXVI. 
Reflex  Neuroses 752 

CHAPTER  XXVII. 

Infections  of  and  from  the  Mouth,  and  Sterilization      ....     766 


DENTAL  PATHOLOGY  AND  THERAPEUTICS. 

SECTION  I. 

GENERAL  PATHOLOGY. 

CHAPTER  I. 
GENERAL  PRINCIPLES. 

General  pathology  {pathos,  disease,  and  logos,  a  discourse)  is  that 
branch  of  science  which  treats  of  the  modifications  in  function  and 
changes  in  structure  occurring  in  disease.  It  embraces  all  patho- 
logical processes  occurring  in  the  human  body,  and  as  many  of  these 
occur  in  and  about  the  teeth,  modified  only  by  the  peculiar  anatomy 
of  the  parts,  Dental  Pathology  may  be  said  to  be  that  branch  of 
dental  science  which  treats  of  modifications  in  function  and  changes 
in  structure  occurring  in  the  diseases  of  the  teeth  and  associate  parts. 

This  being  true,  it  follows  that  the  study  of  dental  pathology  must 
be  preceded  by  a  study  of  the  general  disease  processes  which  affect 
the  tissues  of  the  body,  and  such  of  these  as  are  applicable  to  the 
study  are  known  as  the  General  Principles. 

The  word  Therapeutics  is  derived  from  the  Greek  therapeuin,  to 
take  care  of,  meaning  the  measures  adopted  to  remedy  or  remove 
the  changes  induced  by  pathological  processes. 

The  study  of  the  pathology  of  a  part  begins  with  a  study  of  its 
anatomy  and  histology,  then  naturally  follows  a  study  of  its  physi- 
ology and  embryology.  These  form  the  basis  from  which  degrees 
of  abnormal  function  and  altered  structure  may  be  judged  by  com- 
parison with  similar  processes  occurring  in  other  parts  of  the  body. 

The  body  is  composed  of  cells  held  together  by  intercellular  sub- 
stance. These  cells  are  the  essential  functionating  parts  of  the 
organism;  each  cell  is  composed  of  a  small  mass  of  protoplasm 
containing  in  nearly  all  cases  a  nucleus,  and  has  a  form  adapted  to 
2  (17) 


18  GENERAL  PRINCIPLES 

its  environment  and  function.  The  exact  chemical  composition  of 
protoplasm  is  unknown  and  efforts  at  analysis  destroy  its  peculiar 
property  as  a  substance  exhibiting  a  sequence  of  phenomena  called 
life.  It  is  a  viscid  substance  composed  physically  of  a  network,  the 
spongioplasm,  containing  a  slightly  more  fluid  substance,  the  hyalo- 
plasm.^ Chemically  it  is  70  per  cent,  water  containing  a  collection 
of  proteids,  and  differs  as  to  these  in  the  different  classes  of  cells. 
Proteids  are  but  imperfectly  understood,  but  are  known  to  consist 
essentially  of  carbon,  hydrogen,  oxygen,  and  nitrogen,  combined 
with  sulphur  and  other  varying  elements  in  enormous  molecules 

approximately  represented  by  the  formula 
Fig-  1  C400H310O120N50S.2     This  formula  represents 

merely  the  quantities  of  these  elements, 
which  are  probably  combined  into  various 
chemical  compounds  in  the  cell,  including 
in  some  proteids  one  or  more  carbohydrate 
radicals,  and  each  having  its  peculiar 
chemical  affinity  for  food  materials,  and 
even  irritating  or  poisonous  materials, 
capacity  for  energy  or  function,  and  reduc- 
Changes  of  form  in  an     ^j^^  to  waste  or  usclcss  Cell  material.     The 

ameba:    FF,    pseudopodia;  i  p     i  •  p        n 

V,  vesicle;  N,  nucleus.  study  ot  the  properties  01  cell  protoplasm 

may  be  made  by  observing  in  situ  the 
action  of  living  cells  under  normal  conditions,  and  when  subjected 
to  artificial  stimuli,  and  by  observing  the  action  of  free  single  cells, 
such  as  an  ameba,  under  like  conditions. 

If  a  drop  of  water  be  taken  from  the  sides  or  bottom  of  an  aqua- 
rium, placed  on  a  slide  and  covered  with  a  cover-glass,  and  then 
placed  under  a  microscope  with,  first,  a  Y'  objective,  there  will  be 
noted  at  some  portion  of  the  fluid  a  small  transparent  mass  having 
the  appearance  of  a  colorless  fragment  of  jelly;  this  is  an  ameba. 
The  outline  of  the  mass  may  have  almost  any  form.  At  some  por- 
tion there  will  be  a  defined  and  easily  distinguished  spot,  the  nucleus; 
at  another  point  a  vesicle  is  seen;  the  body  of  the  ameba  appears  to 
contain  numbers  of  fine  granules.  The  nucleus  appears  more  mark- 
edly granular  than  the  body  of  the  ameba.  If  kept  under  obser- 
vation, the  ameba  will  be  seen  to  change  its  outlines;  at  one  or  more 
and  it  may  be  in  several  places,  projections  like  blunt  arms  or  feet 
are  seen  to  be  extending  from  the  ameba  (Fig.  1).  On  account  of 
their  appearance  they  are  called  by  the  physiologist  pseudopodia, 
from  pseudo,  false,  and  pous,  a  foot — false  feet.     These  changes  of 

1  Kirke's  Physiology.  2  Schofield,  Elementary  Physiology. 


PROPERTIES  OF  CELLS 


19 


form  are  much  varied  (Fig.  2),  The  cell  has,  therefore,  the  property 
of  altering  its  form — i.  e.,  it  has  mobility  and  contractility;  as  by 
means  of  these  motions  it  changes  its  location,  it  has  the  property 
of  locomotion. 

Fig.  2 


Ameboid  movement  of  a  white  blood  corpuscle  of  man ;   A^arious  phases  of  movement . 

(Klein.) 

When  certain  solid  substances  contained  in  the  water  come  in 
contact  with  the  ameba,  the  latter  is  seen  to  flow  around  and  engulf 
them;  as  is  shown  in  Figs.  3  and  4,  where  the  analogue  of  an  ameba, 
a  leukocyte,  has  taken  in  bacteria  (phagocytosis).  After  a  time  the 
ingested  body  is  found  to  have  disappeared;  it  has  been  digested. 
Evidently  the  cell  must  produce  a  substance  capable  of  dissolving 
some  foreign  substances — i.  e.,  it  has  the  function  of  secretion.  This 
is  due  to  a  digestive  enzyme  analogous  to  trypsin,  which  has  been 
experimentally  isolated   from   the   ameba. ^     More  than  this,   the 


Fig.  3 


Fig.  4 


Leukocyte  of  a  frog  from  the  neighborhood 
of  a  piece  of  the  lung  of  a  mouse  infected  with 
anthrax,  about  forty-two  hours  after  the  piece 
of  lung  had  been  placed  under  the  skin  of  the 
frog's  back.  The  leukocyte  is  in  the  act  of  eat- 
ing up  an  anthrax  bacillus.  (Brunton,  after 
Metchnikoff.) 


The  san:ie  leukocyte  a  few 
minutes  later,  after  it  has  com- 
pletely enveloped  the  bacillus. 
(Brunton,  after  Metchnikoff.) 


ameba  does  not  take  in  substances  indiscriminately;  some  it  rejects. 
All  cells  change  the  chemical  nature  of  the  media  in  which  they 
grow,  both  by  exhausting  the  nutritive  supply  and  ejecting  their 
excreta. 

If  the  temperature  of  the  slide  be  raised  the  movements  of  the  cell 
become  more  rapid,  and  if  raised  to  a  temperature  of  55°  C.  the 
cell  contracts  in  a  round  lump;  it  responds  to  stimuli,  and  has 
therefore  the  property  of  irritability. 

If  the  stage  be  cooled,  the  movements  of  the  protoplasm  are 


1  Hiss  and  Zinsser,  Text-book  of  Bacteriology. 


20 


GENERAL  PRINCIPLES 


lessened,  and  when  foreign  substances  come  in  contact  with  the 
cell  it  fails  to  encompass  them — its  irritability  and  contractility 
are  lessened. 

It  is  noted  that  some  simple  cells  are  attracted  and  stimulated  by 
light;  others  are  repelled  by  it. 

If  a  mild  induction  (interrupted)  current  be  passed  through  the 
water  in  which  the  ameba  is,  the  movements  of  the  cells  are  checked ; 
if  a  strong  current  be  passed,  the  cell  contracts  sharply.  If  a  gal- 
vanic (constant)  current  be  passed,  movement  at  first  ceases,  but 
pseudopodia  are  extruded  toward  the  cathode  and  the  cell  crawls 
toward  that  pole.^ 

Fig.  5 


Forms  assumed  by  a  nucleus  in  dividing:  a,  resting  nucleus;  b,  skein-form,  open 
stage;  c,  wreath-form;  d,  aster,  or  star-form;  e,  equatorial  stage  of  division;  /,  separa- 
tion more  advanced;  g  and  h,  star  and  wreath  forms  of  daughter  nuclei.  (Reduced 
from  Flemming's  drawings  in  the  Arch.  f.  Mik.  Anat.) 

The  cell  responds  to  mechanical  stimuli,  such  as  violent  shaking, 
by  contraction." 

If  substances  such  as  ether  or  chloroform  are  added  to  the  fluid, 
the  irritability  of  the  cell  is  so  lessened  that  it  does  not  respond  to 
stimuli.    It  is  either  chilled  by  evaporation  or  actuall}^  anesthetized. 

If  the  supply  of  oxygen  be  cut  off,  or  if  carbon  dioxid  be  admitted 
to  the  fluid,  movement  ceases  and  the  cell  remains  contracted. 

If  the  observations  are  continued,  it  will  be  noticed  that  changes 
occur  in  the  nucleus  of  the  cell.  A  series  of  alterations  in  its  figure 
are  noted,  as  shown  in  Fig.  5.  Two  nuclei  are  formed,  and  soon  the 
body  of  the  cell  divides  and  two  cells  appear — the  ameba  has  repro- 
duced itself. 

These  observations  serve  to  show  that  protoplasm  as  shown  by 
the  behavior  of  cells  containing  it  has  the  properties  of  irritability, 
contractility,  motion,  selection,  secretion,  and  excretion  (i.  e.,  met- 


1  O.  Hertwig,  The  Cell. 


2  Ibid. 


PROPERTIES  OF  CELLS  21 

abolism  or  cell  digestion)  and  reproduction,  and  that  it  responds  to 
stimuli  of  physical  and  chemical  nature,  and  that  its  functions  may 
be  altered  l)y  substances  which  are  })rought  in  contact  with  it. 
Upon  these  facts  depends  the  practice  of  therapeutics,  in  which 
stimulation,  sedation  or  alteration  of  nutritive  function  of  the  cells 
by  means  of  the  various  drugs  or  remedies  available  is  the  aim  of 
the  therapeutist. 

A  living  organism,  it  will  be  seen,  has  a  certain  degree  of  action 
and  function.  The  general  average  of  its  action  and  functions  is 
spoken  of  as  a  condition  of  health.  When  from  any  cause  the  func- 
tions are  raised  or  lowered  or  in  any  way  chemically  altered  from 
the  general  average,  a  condition  of  disease  exists. 

Stimulation. — Certain  agencies  applied  to  the  cell  increase  its 
activity;  this  is  called  stimulation.  The  movements  of  the  cell 
become  more  rapid,  food  particles  are  taken  in  more  rapidly  and 
disappear  more  quickly;  irritability,  contractility,  and  secretion  are 
increased.  The  cell  subdivides,  or  reproduces  more  quickly.  In- 
crease the  stimulation,  and  the  vital  activity  becomes  fretful;  in 
some  cases  cell  division  is  incomplete — the  nucleus  divides,  but  not 
the  cell  body.  Increase  the  stimulation  beyond  this  degree,  and  the 
wearied  cell  ceases  its  movements^ — refuses  to  respond;  is  paralyzed 
in  the  body  by  overwork.  It  has  also  been  shown  that  the  cell 
loses  its  essential  substance  in  overwork  and  that  sometimes  the 
products  of  its  activity  are  held  about  it,  causing  cessation  of 
function.  This  may  be  restored,  if  not  carried  too  far,  by  rest  and 
nutrition  or  by  rest  and  the  removal  of  the  waste  product. 

Sedation. — If  the  conditions  be  reversed;  if,  instead  of  applying 
a  stimulus  to  the  cell,  an  opposite  influence  be  introduced,  the 
phenomena  are  reversed. 

If  the  temperature  be  reduced,  the  movements  of  the  cell  become 
sluggish;  the  body  changes  its  form  more  slowly  and  less  extensively 
— i.  e.,  contractility  is  lessened;  particles  taken  into  the  cell  remain 
apparently  unchanged;  irritability,  secretion,  and  excretion  are 
lessened;  and,  furthermore,  reproduction  does  not  occur  nearly  so 
rapidly — that  is,  the  cell  in  contact  with  sedative  influences  has  all 
of  its  activities  lessened.  This  leads  to  paralysis  and  death  of  the 
cell — it  is  starved  to  death. 

Alteration. — It  is  to  be  understood  that  the  cell  is  a  microscopic 
laboratory  conducting  complex  chemical  processes  which  may  be 
altered  by  an  infinite  number  of  influences  of  subtle  nature.  This 
modification  may  possibly  occur  in  a  manner  not  referable  to  simple 
stimulation  or  sedation,  as,  for  example,  by  retention  of  waste,  or 
depositon  of   matter  extraneous  to  the  cell.      Such   changes  may 


22  GENERAL  PRINCIPLES 

fittingly  be  spolven  of  as  alterations,  especially  in  view  of  the  behavior 
of  cells  when  subjected  to  the  influence  of  that  class  of  drugs  known 
as  alteratives  or  such  influences  as  sunlight  or  the  psychological 
remedies.  While  such  alterations  also  probably  occur  as  the  result 
of  stimulation  and  sedation,  the  fact  that  the  beneficial  action  of 
certain  classes  of  therapy  is  not  understood  warrants  this  third 
classification  even  if  for  explanatory  reasons  only.  The  term  mal- 
nutrition is  synonymous  with  alteration  as  here  described. 

Every  cell  has  a  range  of  resistance  to  these  influences  which  tend 
to  destroy  it,  which  is  fitly  termed  the  resistance  of  vitality.  Disease 
itself  is  some  alteration  in  the  cell  chemistry  controlling  any  one  or 
more  of  these  several  cell  properties,  of  irritability,  contractility, 
growth,  secretion,  maintenance,  or  reproduction.  If  any  one  of 
these  properties  is  not  exhibited,  it  is  said  that  the  cell  is  diseased. 

The  cell  lives  its  cycle  and  reproduces,  and  the  parent  is  no  more, 
the  life  being  continued  in  the  offspring. 

The  life  and  properties  of  this  small  mass  of  protoplasm  represent 
in  miniature  the  primitive  functions  and  life  of  the  highest  animals. 

The  contractility  is  represented  in  the  motive  apparatus  of  the 
higher  animals. 

The  reception,  engulfing,  and  dissolving,  or  casting  out,  of  bodies 
with  which  the  ameba  is  brought  in  contact  correspond  in  the  higher 
animals  to  the  digestive  apparatus  and  process  and  the  excretory 
function. 

The  highly  evolved  irritability  is  represented  in  the  nervous 
system  of  the  higher  animals. 

The  movements  occurring  in  and  about  the  vacuole  are  the  pro- 
genitors of  the  circulatory  apparatus  and  all  of  its  adjunct  organs. 

If  the  irritability  of  a  simple  cell  be  increased  or  diminished,  it 
corresponds  to  a  disease  of  the  nervous  system,  and  so  with  the 
other  functions. 

In  the  human  body  certain  collections  of  cells  are  found  in  which 
one  function  is  active,  the  others  in  abeyance;  thus,  large  colonies 
of  cells  exist  in  which  contractility  is  the  dominant  property  noted; 
these  are  muscle  cells.  Others  have  but  the  property  of  irritability; 
these  are  nerve  cells.  Still  others  develop  peculiar  chemical  func- 
tions, and  become  glandular  or  secretory  cells.  Such  collections  of 
cells  are  known  as  tissues.  These  special  cell  colonies  or  tissues  are 
built  together  into  defined  masses  for  the  performance  of  their 
specialized  functions.  In  the  development  of  these  masses,  means 
of  holding  and  maintaining  the  cells  in  definite  mass  forms  and 
provisions  for  their  food  supply  and  waste-removing  apparatus 
are  provided  in  what  are  called  the  connective  tissues,  binding  the 


NUTRITION  23 

cells  in  definite  forms  and  transmitting  their  vascular  supply  (food- 
and  waste-carrier).  When  thus  bound  together  the  tissues  are  said 
to  form  organs. 

While  all  tissues  are  capable  of  analysis  into  cells  and  intercellular 
substance,  a  more  practical  view  may  resolve  the  tissues  into  (1)  func- 
tional cells;  (2)  a  supporting  intercellular  substance;  (3)  intercellular 
spaces  in  which  flows  the  lymph  derived  from  the  blood;  (4)  the 
channels  of  circulation  and  conductors  of  nervous  impulses — i.  e., 
arteries,  capillaries,  veins,  lymphatics,  and  nerves.  The  arteries 
bring  to  the  tissues  the  blood  freighted  with  oxygen  and  nutrient 
material.  As  it  passes  "through  the  capillaries  a  portion  of  the  blood 
plasma,  under  arterial  pressure  and  osmotic  force,  passes  into  the 
intercellular  spaces  into  contact  with  the  cells.  This  exuded  fluid 
is  now  called  lymph. 

Stated  in  general  terms,  the  food  materials  contained  in  arterial 
blood  and  furnished  to  the  tissues  by  way  of  the  lymph  are  water, 
some  proteid,  and  the  constituent  to  make  proteid,  amino-acids  and 
polypeptids,^  glucose  and  fats  or  their  elements,  inorganic  salts, 
and  oxygen.  From  this  store  the  cells  take  what  they  require,  and 
within  themselves  they  elaborate  chemically  substances  essential  to 
their  growth  and  maintenance  as  masses  of  functionating  protoplasm 
(anabolism).  As  the  protoplasm  is  of  more  complex  composition 
than  the  majority  of  food  elements,  they  are  said  to  form  from  simple 
compounds  substances  of  a  higher  degree  of  complexity.  Having 
performed  its  functions,  or  in  the  act  of  such  performance,  this 
protoplasm  is  chemically  altered  into  waste  products  of  less  complex 
chemical  composition  (catabolism)  and  such  "products  of  catabo- 
lism"  are  thrown  out  from  the  cell  into  the  lymph  in  the  inter- 
cellular (lymph)  spaces.  This  process  may  be  spoken  of  as  cell 
elimination  and  the  substances  themselves  as  cell  ejecta.  The  total 
process  is  termed  metabolism. 

While  the  exact  nature  of  the  chemical  change  occurring  in  cells  is 
not  known,  the  present  thought  is  that  much  of  the  process  of  cell 
metabolism  is  conducted  within  the  cell  through  the  action  of  one 
or  more  enzymes  which  have  the  power  of  catalytically  effecting 
prompt  and  smooth  chemical  changes  at  low  temperature,  which  can 
at  times  be  produced  in  the  laboratory  only  by  complicated  experi- 
ments not  at  all  comparable  with  the  action  of  cells. 

Various  organs  of  the  body  evidently  prepare  the  food  material 
absorbed  by  the  intestines  for  the  use  of  the  cells — for  example,  gly- 
cogen is  formed  from  the  absorbed  glucose  by  the  ferment  of  liver 

1  Howell,  Text-book  of  Physiology,  1911,  p.  877. 


24  GENERAL  PRINCIPLES 

cells,  and  when  needed  again  is  transformed  into  glucose.  As  a 
proteid  example  the  fibrinogen  of  the  blood  is  supposed  to  be  pro- 
duced in  the  liver. ^  The  proteid  as  built  into  complete  form  in  the 
body  juice  and  tissues  is  very  complex  and  may  contain  all  or  a 
portion  of  fourteen  or  more  monoamino-acids  or  four  or  more 
dikmino-basic  bodies,  which  shows  the  tremendous  problem  of  the 
chemical  study  of  metabolism,  which  is  as  yet  imperfect.^ 

Ehrlich's  side-chain  theory  for  immunity  (which  see)  presupposes 
the  presence  of  atom  groups  of  protoplasm  surrounding  a  complex 
group  of  atom  groups,  the  nucleus,  each  atom  group  having  aflfinity 
for  a  particular  form  of  substance  presented  to  it.  These  he  terms 
receptors,  and  each  is  supposed  to  possess  a  combining  or  prehending 
group  of  atoms  called  an  haptophorous  group  and  a  ferment  group 
capable  of  altering  the  chemistry  of  the  food  element  to  suit  its  needs 
or  that  of  the  cell  as  a  whole;  this  latter  group  is  termed  a  zymoph- 
orous  group.  This  obviously  is  merely  stating  in  a  scientific  manner 
that  the  cell  receives  and  digests  food  materials.  The  carbohydrates 
and  fats  are  in  the  main  the  producers  of  energy,  and  are,  lastly, 
resolved  into  glucose  and  fat  or  their  elements  for  the  consumption 
of  the  cells,  and  by  them  appropriated  into  their  protoplasm,  whence, 
by  catabolic  changes,  they  are  started  upon  their  retrogressive 
course  to  the  final  products  CO2  and  water.  The  proteids  are  mainly 
useful  for  the  building  of  the  cell  protoplasm  and  its  maintenance, 
and  when  catabolized  end  in  products  which  in  other  organs  are 
transformed  into  urea  and  uric  acid. 

There  is  evidence  that  changes  occur  in  the  cell  waste  either  in  the 
blood  or  in  various  organs  of  the  body.  While,  then,  the  bodily  ejecta 
contain  substances  fairly  constant  in  composition,  they  are  held  to 
represent  elaborations  of  cell  waste  rather  than  actual  cell  ejecta. 
For  example,  urea  is  pretty  certainly  derived  from  muscular  tissue, 
yet  is  nearly  absent  in  muscle  and  is  supposed  to  be  due  to  the  dehy- 
dration of  ammonium  carbonate  in  the  liver.^  Lactic  acid  and  ammo- 
nium carbonate  have  been  experimentally  shown  to  be  probably  com- 
bined into  uric  acid  in  the  liver.  The  cell  waste  is  carried  by  the 
lymph  into  the  lymphatics  connecting  with  the  intercellular  spaces. 
Thence  it  is  delivered  by  way  of  the  venous  system  to  the  circulation, 
for  further  elaboration  and  elimination  from  the  body.  Any  inter- 
ference with  such  elaboration  or  elimination  must  of  necessity  result 
in  a  retention  of  waste  products  within  the  system,  probably  leading 
to  irritation  and  disturbance  of  metabolism  in  all  cells. 

Cell  metabolism  is  a  chemical  change  and  is  therefore  accompanied 

1  Howell,  Text-book  of  Physiology,  1911,  p.  444.  ^  ibjd.,  p.  986. 

'  Kirke's  Physiology. 


NUTRITION  25 

by  lieat  production.  Energy  is  stored  up  in  the  cell  as  latent  force 
existing  in  actual  cell  substance  and  is  capable  of  liberation  under 
stimulus,  which  force  is  expressed  in  various  forms  of  functional 
activity — i.  e.,  contractility  in  muscular  tissue,  irritability  and  men- 
tality in  nervous  tissue,  secretion  in  the  various  secretory  glands, 
eliminative  selection  in  the  various  excretory  organs,  etc.  Experi- 
mental evidence  has  shown  that  after  energy  has  been  liberated  to 
the  point  of  fatigue,  there  is  an  actual  loss  of  substance  by  the  cells, 
in  consequence  of  which  they  become  smaller  and  of  different  his- 
tological appearance.  It  is  evident,  therefore,  that  any  condition 
which  will  produce  an  expenditure  of  energy  without  a  compensating 
restoration  of  cell  material  must  result  in  a  malnutritional  process. 
Cells  after  a  period  of  activity  undergo  degenerative  processes, 
and  are  removed  or  are  reproduced  by  the  process  of  mitosis 
(Fig.  5).  _ 

The  life  conditions  of  cells  are  necessarily  those  under  which  they 
best  perform  these  functions  without  exhaustion,  and  are  the  fol- 
lowing: (1)  a  proper  food  supply,  including  water  and  oxygen;  (2) 
a  proper  removal  of  waste  products;  (3)  proper  physical  conditions, 
including  a  proper  temperature;  (4)  possibly  a  proper  innervation.^ 
Any  interference  with  these  conditions,  which  may  be  termed  the 
normal  physiological  conditions,  results  in  a  morbid  process  of 
physiology  or  pathology  in  its  limited  sense.  With  such  interfer- 
ence disease  may  be  said  to  begin.  The  definition  of  disease  as 
an  alteration  of  nutrition  is  therefore  appropriate.  For  this  reason 
the  proximate  exciting  causes  of  disease  are  classed  as  (1)  abnormal 
food  supply;  (2)  abnormal  waste  removal;  (3)  abnormal  physical 
conditions;  (4)  abnormal  nerve  supply. 

The  morbid  physiology  results  in  morbid  products  or  in  retained 
normal  products  and  an  altered  cell  function.  When  pronounced 
this  is  spoken  of  as  Functional  Disease,  although  it  may  be  said  to 
be  in  existence  even  if  discomfort  be  not  produced.  Sooner  or  later 
an  abnormal  change  in  the  histological  characteristics  of  the  cells 
or  intercellular  substance  may  occur,  which  has  been  referred  to  as 
Morbid  Histology  or  Pathological  Histology.  As  definite  micro- 
scopic and  often  macroscopic  appearances  are  associated  with  certain 
diseased  conditions,  these  are  referred  to  as  the  Morbid  Anatomy  of  a 
disease  or  Pathological  Anatomy.  The  phemonena  associated  with  a 
disease  are  called  its  Semeiology  {semeion,  a  mark  or  sign)  or  Symp- 

1  While  this  conception  is  practical,  experiments  at  the  Rockefeller  Institute  have 
shown  that,  kept  in  a  proper  aseptic  nutritive  fluid  at  a  low  temperature  various 
organs  and  tissues  may  be  preserved  for  a  considerable  time  and  even  shipped,  thus 
being  available  for  surgery.  This  shows  that  cells  possess  a  life  only  dependent  upon 
the  body  as  a  whole  for  their  source  of  nutritive  supply. 


26  GENERAL  PRINCIPLES 

tomatology,  and  are  either  described  by  the  patient  as  sensations  or 
pains  of  varied  character  or  situation  (Subjective  Symptoms),  or  may 
be  noted  by  normal  or  aided  vision,  by  physical  examination, 
chemical  analysis  or  positive  reactions  to  certain  biological  tests 
(as  in  the  Wassermann  reaction  for  syphilis)  (Objective  Symptoms). 
That  which  excites  a  disease  or  promotes  the  action  of  the  excitation 
is  called  a  Disease  Cause.  The  study  of  disease  causes  is  Etiology 
(aetios,  a  cause,  and  logos).  It  is  noted  that  diseases  having  a  fairly 
defined  pathology  and  morbid  anatomy  have  from  their  beginning 
to  ending  tolerably  constant  phenomena;  they  have  each  a  natural 
history;  this  is  called  the  Clinical  History  of  a  disease. 

The  study  of  the  origin  and  development  of  a  disease  together  is 
known  as  its  Pathogenesis  (pathos,  disease;  gennao,  I  produce). 
Through  the  study  of  the  characteristic  symptoms  of  diseases,  as 
well  as  those  common  to  several  diseases,  a  particular  disease  may  be 
distinguished.  This  is  called  Diagnosis  {dia,  through;  gignosko,  I 
know) — Direct  Diagnosis  when  there  is  no  question  as  to  the  symp- 
toms, Differential  Diagnosis  when  several  diseases  are  possible  and 
the  characteristics  of  one  are  considered  as  more  pronounced.  Under 
certain  circumstances  a  disease  may  be  inferred  to  be  present  by 
excluding  all  other  possible  conditions  (Diagnosis  by  Exclusion).  A 
fourth  method  of  diagnosis  is  by  the  therapeutic  test  (see  below).  In 
the  course  of  a  disease  experience  has  shown  that  certain  signs  and 
symptoms  are  apt  to  be  followed  by  good  or  ill  results,  as  the  case 
may  be.  By  these  signs  and  symptoms  it  may  be  foretold  with  some 
degree  of  assurance  what  will  be  the  probable  outcome  of  the  disease. 
The  inference  based  upon  these  symptoms  is  known  as  the  Prognosis 
(pro,  before,  and  gignosko,  I  know).  The  care  of  or  treatment  of  a 
disease  is  its  Therapeutics.  This  involves  a  knowledge  of  remedies 
applicable,  known  as  the  Materia  Medica.  When  applied  upon  the 
basis  of  a  scientific  study  of  the  pathogenesis,  clinical  history,  and 
prognosis  of  disease  and  a  parallel  knowledge  of  the  physiological 
action  of  drugs  and  of  other  remedies,  the  treatment  is  known  as 
Rational  Therapeutics.  When  the  treatment  is  based  upon  the 
known  good  effects  of  a  remedy  in  a  certain  disease,  and  not  upon 
its  physiological  action,  it  is  known  as  Empirical  Therapeutics. 
Diagnosis  may  not  always  be  clear,  but  upon  a  basis  of  previous 
experience  of  association  of  symptoms  a  given  therapeutics  may 
be  applied  with  more  or  less  rationality.  Whether  good  results 
follow  or  not  the   method  is   known  as   "the   therapeutic   test." 

The  pathogenesis  of  a  disease  being  known,  intelligent  efforts  may 
be  exerted  for  its  prevention.  The  causes  may  be  removed  or  neutral- 
ized before  they  have  an  opportunity  to  act;  this  is  Prophylaxis. 


NUTRITION  27 

The  science  of  prevention  of  disease  up(jn  the  broad  basis  of  a 
knowledge  of  disease  causes  and  observance  of  laws  of  health  is 
Hygiene. 

It  will  be  seen  that  a  knowledge  of  special  pathology  can  only  be 
obtained  from  (1)  a  knowledge  of  pathology  in  general  or  at  least  of 
those  principles  of  general  pathology  which  underlie  all  disease  pro- 
cesses; (2)  a  knowledge  of  the  local  anatomy  and  histology;  (3)  a 
knowledge  of  local  embryology  and  physiology;  (4)  a  study  of  local 
pathology  and  morbid  anatomy.  To  this  must  be  added  a  study  of 
materia  medica  and  special  therapeutics. 


CHAPTER  II. 
CAUSES  OF  DISEASE,   GENERAL  AND  LOCAL. 

A  DISEASE  cause  may  be  defined  as  any  influence  of  whatsoever 
nature  which  is  capable  of  disturbing  the  nutritive  balance  of  any 
portion  of  the  body.  The  branch  of  study  which  deals  with  the  causes 
of  disease  is  called  Etiology. 

The  causes  of  disease  are  classed  as  Exciting  (or  Determining) 
and  Predisposing.  These  are  each  divisible  into  Extrinsic,  originating 
from  without,  and  Intrinsic,  originating  within  the  body. 

EXCITING   CAUSES    OF   DISEASE. 

These  are  influences,  either  extrinsic  or  intrinsic,  which  are  com- 
petent to  suddenly  or  gradually  interfere  with  the  nutrition  of  the 
cells  of  a  part  or  with  the  general  nutrition  of  cells.  These  influ- 
ences are  very  numerous,  but  may  be  grouped  according  to  their 
action  under  a  few  convenient  headings:  (1)  Abnormal  Food  Supply. 
(2)  Abnormal  Waste  Removal.  (3)  Abnormal  Physical  Conditions. 
(4)  Abnormal  Nerve  Supply. 

These  are  termed  the  Proximate  Exciting  Causes,  as  their  effects 
are  immediately  exerted  upon  the  cells.  Other  causes  may  be  back 
of  these  and  are  spoken  of  as  Primary  (or  Contributory)  Causes — 
e.  g.,  tuberculosis  of  the  lung  (primary)  may  cause  insufficient 
oxygenation  of  the  blood  which  constitutes  an  abnormal  food  supply 
(proximate). 

Abnormal  Food  Supply. — By  abnormal  food  supply  is  meant  an 
altered  quantity  or  quality  of  nutritive  elements  delivered  to  the 
cells  either  of  a  part  or  of  the  entire  body.  The  primary  causes  of 
this  may  exist  as  disturbances  or  faults  in  any  of  the  food-elaborating 
organs,  the  lungs,  the  eliminating  organs,  or  the  oxygen  carriers  of 
the  blood  may  exist  in  lessened  numbers.  In  the  first  case  the  quality 
or  quantity  of  nutritive  material  is  impaired,  in  the  second  and  fourth 
cases  oxygenation  is  insufficient,  and  in  the  third  case  materials  in- 
jurious to  cells  are  retained  in  the  body  and  are  again  presented  as 
food  to  the  cells,  acting  as  poisons.  Poisonous  or  even  non-poisonous 
drugs,  and  the  products  of  bacterial  action,  Avhether  absoibed  from 
the  intestines  or  from  foci  of  infection,  have  all  more  or  less  delete- 
(28) 


EXCITING  CAUSES  OF  DISEASE  29 

rioiis  action  upon  cell  protoplasm,  violent  if  entering  the  blood  in 
large  quantity,  chronic  if  entering  continuously  in  small  quantities. 

Faults  in  the  circulatory  apparatus,  interfering  with  the  circulation 
generally,  cause  an  interference  Avith  general  nutrition,  while  local 
disturbances  of  the  circulation  from  any  cause  disturb  the  relations 
of  the  blood  supply  to  the  nutrition  of  a  part.  Thus  the  fresh  blood 
supply  (food  supply)  to  a  particular  location  may  be  excessive,  as 
in  arterial  hyperemia,  or  deficient,  as  in  venous  hyperemia  and 
inflammation. 

Abnormal  Waste  Removal. — Abnormal  waste  removal  is  ordinarily 
included  under  the  heading  of  abnormal  food  supply,  and  it  is 
evident  that  retention  of  waste  in  the  blood  causes  the  presentation 
to  cells  of  an  abnormal  food  or  poison.  In  local  conditions,  such  as 
venous  hyperemia  and  inflammation,  the  stasis  causing  waste  reten- 
tion prevents  the  access  of  a  fresh  food  supply  as  well.  In  kidney 
disease  the  substances  ordinarily  physiologically  eliminated  by  the 
kidneys  are  retained  in  the  blood  and  act  as  poisons  to  cell  proto- 
plasm generally.  Insufficient  circulation  of  lymph  about  cells 
means  a  relative  retention  of  waste  products  about  the  cells  with 
its  effects  upon  them. 

Abnormal  Physical  Conditions. — This  class  of  disease  causes 
includes  all  injuries  due  to  any  of  the  physical  or  chemical  forces: 
Traumatic  injuries,  such  as  cuts,  bruises,  surgical  openings,  etc. 
Mechanical  causes,  such  as  compressions,  obstructions  to  ducts  or 
the  natural  outlets  of  the  body,  faults  in  the  circulatory  mechanism, 
stoppages  in  the  arteries  or  veins.  Chemical  causes,  such  as  the 
action  of  abnormal  temperatures,  burns,  freezing,  or  irritations  of 
various  sorts,  such  as  those  due  to  mustard,  arsenic,  acids,  or  caustics, 
and  the  local  effects  of  microorganisms  may  all  be  classified  under 
this  heading.  The  disturbance  is  due  to  either  a  direct  destruction 
of  the  life  of  the  cells  or  an  interference  with  the  circulation  in  a  part. 

Abnormal  Nerve  Supply. — It  is  known  that  division  of,  injury  to, 
or  disease  of  certain  nerves  causes  trophic  or  nutritional  changes  in 
the  part  to  which  they  are  supplied.  Whether  the  nutrition  of  the 
parts  is  controlled  by  special  trophic  nerve  fibers  has  not  been 
demonstrated.  Halliburton/  in  support  of  the  trophic  influence 
of  nerves,  instances  that  when  the  fifth  nerve  (sensory)  is  divided 
beyond  the  Gasserian  ganglion,  ulceration  of  the  cornea  results; 
while  if  the  seventh  nerve  (motor)  be  divided  or  paralj^zed,  the  eye- 
ball is  equally  exposed  to  irritants,  yet  does  not  ulcerate.  He  also 
instances  that  division  of  the  vagi  produces  fatty  degeneration  of 
the  heart. 

'  Kirk's  Physiologj\ 


30  CAUSES  OF  DISEASE,  GENERAL  AND  LOCAL 

While  admitting  the  lack  of  anatomical  proof,  he  regards  the 
trophic  influence  of  nerves  upon  parts  to  be  unexplainable  upon 
the  ground  taken  by  others,  that  all  apparently  trophic  changes 
are  due  to  disturbances  of  the  vasomotor  nerves  controlling  the 
caliber  of  vessels.  According  to  these  other  observers  degrees  of 
dilatation  are  produced  which  modify  the  amount  of  blood  delivered 
to  a  part  and  thus  modify  its  nutrition. 

Effects  are  produced  upon  nutrition  by  causes  which  can  act 
only  through  the  nervous  system — e.  g.,  the  effect  of  anxiety  upon 
appetite  and  digestion.  The  interdependence  of  these  classes  of 
causes  is  almost  self-evident;  for  example,  constant  suppuration  at 
a  focus  of  infection  (abnormal  physical  condition)  may  induce  a 
toxemia  (abnormal  food  supply)  which  may  be  responsible  for  kidney 
or  other  disease  (abnormal  physical  condition),  resulting  in  the 
retention  of  waste  products  in  the  blood  (abnormal  waste  removal 
or  food  supply),  which  has  a  vicious  result  upon  all  metabolism, 
including  that  of  the  nervous  system,  inducing  in  turn  an  abnormal 
nerve  supply  and  lessening  resistance  even  in  the  tissues  about  the 
original  focus  of  infection.  Such  a  train  of  events  is  known  as  the 
establishment  of  a  vicious  cycle  and  is  interesting  as  related  to  the 
lessened  resistance  produced  in  the  gingival  tissues  in  pyorrhea 
alveolaris. 

PREDISPOSING   CAUSES    OF   DISEASE. 

A  predisposing  cause  of  disease  is  one  which  influences  the  cells 
or  juices  of  the  body  or  part  in  such  a  manner  as  to  lessen  the 
resistance  to  the  action  of  the  exciting  causes  of  disease. 

It  must  be  considered  that  a  predisposition  or  lessened  resistance 
is  in  itself  a  condition  of  disease,  not  recognizable,  perhaps,  yet  a 
departure  from  the  standard  of  the  best  health  of  an  individual  or 
part.  For  the  most  part  predisposition  is  regarded  in  its  relation 
to  the  extrinsic  causes  of  disease,-  such  as  bacterial  influences.  In 
such  a  condition  the  individual  is  said  to  be  susceptible.  {Suscep- 
tibility.)   Predisposition  is  either  general  or  local. 

General  Predisposition. — This  is  either  (1)  a  natural  or  inherent 
lack  of  resistance  to  infectious  or  non-infectious  diseases,  or  (2)  an 
acquired  lack  of  resistance  to  infectious  or  non-infectious  diseases. 
The  human  race  in  general  is  naturally  predisposed  to  many  infec- 
tious diseases,  such  as  tuberculosis,  cholera,  malaria,  measles,  small- 
pox, typhoid  fever,  scarlet  fever,  and  syphilis.^  When  a  person  is 
exposed  to  the  disease  and  contracts  it,  he  is  said  to  be  predisposed 

1  Ziegler,  General  Pathology. 


PREDISPOSING   CAUSES  OF  DISEASE  31 

or  susceptible  to  it.  If  he  does  not  contract  it,  his  system  is  immune 
either  temporarily  or  permanently.  (See  Immunity.)  There  being 
several  forms  of  immunity,  the  lack  of  any  natural  form  may  be 
considered  as  a  predisposition.  This  immunity  is  ordinarily  opera- 
tive when  the  individual  is  in  the  best  state  of  health,  and  when  a 
departure  from  this  standard  is  brought  about  by  any  cause,  exciting 
infective  causes  may  then  act.  This  is  acquired  predisposition. 
Some  individuals  have  a  natural  or  congenital  lessened  resistance 
to  external  influences  of  a  non-infectious  character,  such  as  heat  or 
cold,  mental  effort,  or  nervous  irritations  of  a  degree  ordinarily 
borne  by  the  great  majority  of  individuals.  This  may  also  be  ac- 
quired, as,  for  example,  by  extreme  subjection  to  the  above  or  other 
enervating  causes.  An  inherited  predisposition  to  such  diseases  as 
insanity,  cancer,  or  gout  may  exist. 

Some  persons  cannot  bear  certain  kinds  of  food  without  illness,  or 
react  strongly  to  small  doses  of  drugs,  or  are  not  affected  by  large 
doses.  This  is  called  an  idiosyncrasy,  and  may  be  either  congenital 
or  acquired. 

The  predisposing  causes  capable  of  producing  a  lessened  resist- 
ance may  be  grouped  under  a  few  headings. 

Sex  as  an  Intrinsic  Predisposing  Cause. — In  this  connection  the 
influence  of  sex  upon  predisposition  to  disease  must  be  considered. 
While  the  general  resistive  power  of  the  bodies  of  both  sexes  may 
be  regarded  as  practically  equal  under  similar  conditions,  yet  the 
anatomical  structures  and  physiology  of  each  sex  have  an  influence 
upon  predisposition  to  certain  diseases.  Aside  from  the  diseases 
peculiar  to  sex,  on  account  of  their  peculiar  organs,  each  sex  exhibits 
predispositions  to  diseases  which  the  other  sex  escapes;  for  many 
of  these  the  habits  of  life  furnish  an  explanation,  for  others  an  ex- 
planation is  not  available.  For  example,  males  are  much  more 
subject  to  hemophilia  than  females. 

Age. — During  the  first  two  years  after  birth  the  nervous  system 
and  the  appendages  of  the  alimentary  canal  are  developing,  and 
improper  feeding,  difficult  teething,  or  other  influences  readily  act 
as  exciting  causes  of  alimentary  or  nervous  disturbances. 

Later,  children  are  subject  to  acute  infectious  diseases,  especially 
tuberculosis,  diphtheria,  and  the  eruptive  fevers.  At  adolescence 
other  predispositions  occur,  notably  chlorosis  in  young  girls.  Later 
come  the  diseases  of  early  maturity,  such  as  typhoid  fever,  pulmo- 
nary tuberculosis,  and  to  a  degree  dental  caries. 

In  old  age  or  middle  life  occur  arterial  and  other  degenerations 
and  diseases  consequent  upon  them  or  upon  overstimulation  of 
organs  or  tissues. 


32  CAUSES  OF  DISEASE,   GENERAL  AND  LOCAL 

Temperament. — Temperament  is  the  peculiar  congenital  consti- 
tution of  an  individual  imparting  certain  physical  characteristics 
and  certain  natural  tendencies.    There  are  four  basal  temperaments: 

The  sanguine  is  that  in  which  individuals  are  decidedly  inclined 
to  the  blonde  type,  with  evidence  of  an  abundance  of  the  nutritive 
fluid,  the  blood — i.  e.,  the  vascular  system  is  said  to  dominate  the 
other  functions  of  the  body.  Such  are  predisposed  to  acute  pul- 
monary and  cardiac  diseases  and  inflammatory  disturbances  of 
serious  import.  The  mental  characteristics  of  this  temperament 
are  hopefulness,  cheerfulness,  and  solidity  but  floridity  of  mental 
endowments.    The  recuperative  power  is  good. 

The  bilious  temperament  is  characterized  by  a  decided  inclination 
to  the  brunette  type,  with  evidence  of  a  domination  of  other  func- 
tions by  the  liver.  There  is  a  tendency  to  hepatic  and  digestive 
derangements  and  despondency;  at  the  same  time  there  is  pos- 
sessed great  physical  and  mental  strength,  together  with  a  reliable 
recuperative  power. 

The  nervous  temperament  is  indicated  by  the  smallness  and 
delicacy  of  frame  and  the  quickness  of  motion  and  perception, 
evidencing  a  domination  by  the  nervous  system,  to  diseases  of 
which  such  temperament  predisposes.  In  such  individuals  disease 
is  usually  of  rapid  course,  and  recuperation  is  rather  more  rapid 
than  reliable. 

The  lymphatic  temperament  is  indicated  by  bulk,  pallor,  and  flac- 
cidity  of  tissue,  a  colorlessness  of  temperament,  indicating  an  inherent 
feebleness.  There  is  a  tendency  to  serious  chronic  conditions.  This 
temperament  is  accompanied  by  poor  recuperative  force. 

There  are  no  individuals  of  pure  basal  temperament,  so  that  the 
nearest  approach  is  a  dual  or  binary  temperament,  such  as  the 
biliosanguine,  in  which  the  characteristics  of  the  sanguine  predomi- 
nate, strongly  modified  by  those  of  the  bilious  temperament.  In 
like  manner  the  sanguonervous,  nervolymphatic,  and  other  classes, 
twelve  in  number,  are  recognized  as  having  typical  representatives 
in  each  community.  A  third  or  ternary  classification  is  possible — 
e.  g.,  sanguonervobilious.  It  will  be  seen  that  temperament  has  a 
distinct  relation  to  the  vital  resistance  normally  implanted  in  an 
individual,  and  therefore  may  to  a  certain  extent  be  counted  upon 
in  a  prognosis.  Temperament  is  a  predisposing  cause  probably  only 
in  so  far  as  it  introduces  a  natural  general  lack  of  resistance  to  disease, 
or  irresistibly  drives  an  individual  into  certain  habits  of  life  which 
may  become  the  cause  of  a  lessened  resistance.  The  writer  is  aware 
that  question  has  been  raised  as  to  even  the  existence  of  such  a  thing 
as  temperament.     It  is  true  that  the  Chinese,  Negro,  Arab,  etc.. 


PREDISPOSING  CAUSES  OF  DISEASE  33 

have  not  been  included  in  the  above  classifications.  As  applied 
to  the  Caucasian  race,  however,  what  is  said  above  is  intended  to 
convey  the  meaning  that  there  is  a  combination  of  mental  and 
physical  characteristics  which,  apart  from  education  or  environment, 
influence  the  tendencies  of  individuals. 

Heredity. — Certain  diseases  exhibit  a  predisposition  to  descend 
from  parent  to  child  direct,  or  from  grandparent  through  the  un- 
afi^ected  son  or  daughter  to  a  grandchild  (in  the  latter  case  it  is  called 
atavistic  hereditary  transmission,  also  remote  heredity). 

The  mode  of  transmission  is  in  all  probability  the  inheritance  of 
a  type  of  tissue,  a  tissue  anatomy  and  physiology  which  permit  the 
more  ready  action  of  the  exciting  causes  of  the  disease.  This  ten- 
dency is  called  a  diathesis — e.  g.,  hemorrhagic  diathesis  (hemophilia), 
gouty  diathesis,  or  tuberculous  diathesis.  Diathesis  may  also  be 
acquired.  The  influence  of  race  may  also  be  considered  as  coming 
under  this  heading.     (See  Immunity.) 

Existing  Disease. — The  presence  of  one  disease  may  weaken  the 
resistance  of  a  part  or  the  organism  so  that  another  disease  may 
the  more  readily  become  implanted — e.  g.,  measles  followed  by 
pneumonia;  diabetes  accompanied  by  pyorrhea  alveolaris.  In 
diabetes  the  opsonic  index  may  be  reduced  one-half.  McFarland 
states  that  when  glucose  is  present  in  excess  in  the  blood  (glycosuria 
as  in  diabetes),  susceptibility  to  infection  is  increased. 

Previous  Disease. — At  a  period  subsequent  to  disease  the  same 
disease  may  recur  or  another  disease  may  be  implanted — e.  g., 
pneumonia  predisposes  a  lung  to  a  recurrence  of  pneumonia,  or 
tuberculosis  may  readily  follow.  Previous  disease  may  confer 
immunity  to  the  same  disease,  as,  for  example,  in  smallpox  or 
measles. 

Extrinsic  Predisposing  Causes  of  Disease. — Under  this  head  are 
included  all  those  conditions  of  external  origin  which  lessen  the 
resistance  of  an  individual  to  the  action  of  exciting  causes.  Excessive 
heat  is  weakening;  cold  and  dampness,  by  chilling  the  surface  of 
the  body,  cause  hyperemia  of  internal  parts  and  thus  predispose  to 
such  diseases  as  pneumonia,  rheumatism,  etc.  Fatigue,  unhealthy, 
cramping,  or  sedentary  occupations,  continued  loss  of  sleep  from 
any  cause,  evil  habits,  continued  hunger,  etc.,  are  other  examples  of 
debilitating  influences  wdiich  may  be  partly  intrinsic. 

Local  Predisposition. — Alterations  in  the  normal  physiology  of 
a  part  are  apt  to  occur  through  certain  actions  upon  it,  thus  bringing 
it  into  a  condition  of  lessened  resistance,  permitting  the  action  of 
entirely  different  exciting  causes.  Apart  from  this  fact,  a  part  may 
be  predisposed,  by  nature  apparently,  to  permit  the  growth  of 
3 


34  CAUSES  OF  DISEASE,   GENERAL  AND  LOCAL 

bacteria  which  do  not  grow  well  in  other  tissues.  Local  depression 
of  tissue  vitality  predisposes  to  the  growth  of  organisms  in  the  tissues. 
Thus  slight  injury  producing  either  arterial  or  venous  hyperemia  or 
ischemia  may  permit  bacteria  to  produce  even  grave  consequences. 
More  severe  injury  also  may  predispose,  but  the  contrary  effect  has 
also  been  observed — i.  e.,  that  severe  injury  excites  a  phagocytic 
reaction  and  copious  exudation  of  lymph  (a  later  stage  of  inflamma- 
tion) which  antagonizes  the  bacteria.     (See  Inflammation.) 

The  structure  of  a  part  has  also  been  shown  to  have  an  effect  upon 
the  life  of  microorganisms  gaining  access  to  its  tissues.  The  tissues 
about  the  mouth  are  normally  notoriously  resistant  to  infections, 
but  at  times  are  exceedingly  susceptible,  as  in  pyorrhea  alveolaris. 
Ordinarily  surgical  operations  about  the  mouth  were  successful  in 
pre-aseptic  times,  w^hile  abdominal  or  gynecological  operations  were 
attended  by  an  enormous  percentage  of  death  from  infection. 
General  depression  of  vitality  also  necessarily  affects  the  resistive 
force  of  all  local  tissues.  Thus  extensive  suppuration  is  more  liable 
to  occur  in  those  rendered  feeble  and  anemic  by  any  cause. 

IMMUNITY. 

Immunity  is  the  opposite  of  predisposition,  and,  like  it,  can  be 
either  natural  or  acquired.  It  signifies  an  insusceptibility  to  a  disease. 
Natural  immunity  to  a  particular  infectious  disease  can  only  be 
determined  by  repeated  exposures,  and  may  then  fail  at  last  owing 
to  some  systemic  change,^  Immunity  may  be  exhibited  toward 
only  one  disease.  In  some  persons  disease  appears  to  be  influenced 
by  sex,  as,  for  example,  males  have  a  general  immunity  from  goitre, 
females  from  Addison's  disease.  Immunity  is  influenced  by  age  in 
certain  diseases;  for  example,  the  diseases  of  childhood  are  rare  in 
the  elderly;  they  do  occur,  however.  The  degenerative  diseases  of 
old  age  are  almost  unknown  in  childhood.  Race  has  its  influence; 
the  negro  is  almost  immune  to  malaria  and  yellow  fever,  but  particu- 
larly susceptible  to  smallpox  and  tuberculosis.  Some  have  explained 
this  on  the  ground  that  in  localities  in  which  malaria  and  yellow 
fever  are  endemic  the  disease  has  been  acquired  in  early  life  and 
that  an  apparent  natural  immunity  is  really  an  acquired  immunity. 
Inheritance  of  amboceptors  from  immune  ancestors  has  been  offered 
as  an  explanation.  The  natural  immunity  may  be  more  apparent 
than  real,  owing  to  failure  of  the  bacteria  to  find  a  local  condition 
favorable  to  development  and  to  enter  the  blood.     If  special  care 

1  Green,  Pathology  and  Morbid  Anatomy. 


IMMUNITY  35 

in  experiment  be  taken  to  introduce  the  bacteria,  and  failure  of 
inoculation  result,  the  natural  immunity  is  absolute.  Example: 
Rats  to  diphtheria,  or  negroes  to  j^ellow  fever. 

A  striking  example  of  lost  immunity  occurred  in  the  case  of  a 
friend,  who,  in  early  and  middle  life,  could  handle  poison  ivy  with 
impunity.  On  approaching  seventy  years  of  age,  and  while  in  a 
condition  of  general  debility,  he  was  affected  from  head  to  foot  with 
the  peculiar  dermatitis  as  the  result  of  pulling  up  a  plant. 

The  further  discussion  of  immunity  as  related  to  bacterial  infection 
should  properly  be  discussed  after  the  consideration  of  bacterial 
causes,  and  will  be  found  at  the  end  of  Chapter  III. 


CHAPTER  III. 
MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE. 


The  infectious  and  contagious  diseases  have  for  the  most  part 
been  shown  to  be  caused  by  low  forms  of  vegetable  organisms  known 
collectively  as  fungi,  while  in  a  few  diseases  minute  animal  organisms 
(protozoa)  are  the  causes. 

The  following  table  shows  the  position  of  the  vegetable  organisms 
in  the  scale  of  vegetable  life  and  gives  the  lowest  forms  of  animal 
life: 


Vegetable 
kingdom 


Animal 
kingdom 


Phanerogams: 

plants  reproducing  by  flowers  and  seeds. 
Leafy  cryptogams. 

Cryptogams, 

Thallophytes, 

reproducing 

haying  no  dis- 

Lichens. 

Basidiomycetes. 

Favus  fungi. 

by  spore 

tinction  be- 

Algse. 

Mycomycetes. 

Common  molds. 

formation 

tween  the 

Fungi.     ' 

Phycomycetes. 

Mucor  molds. 

or  division. 

leaf  and  stem.  ^ 

Saccharomycetes. 

Yeasts    or    blasto- 

mycetes. 

Schizomycetes. 

Bacteria. 

Lowest  forms ' 

„                    •     1        11         1  Sarcodinea. 
Protozoa:   single  cells          _,       „  ^ 
.^,      ,    .      ,  ,            J  Flagellata. 
without  circulatory  or  <  „ 

Sporozoa. 
nervous  systems.               ^   , 

[  Infusoria. 

Mycetozoa,    fungi    not    certainly    defined    as 

animal    or    vegetable 

forms.  1 

Higher  forms. 

Certain  insect  an 

i  worm  for 

ms  are  pathogenic. 

Fig.  6 


Trichophyton  tonsurans 
("barbers' itch").  (Myco- 
mycetes.) Diagrammatic. 
(Lehmann.) 


Of  the  protozoa  four  classes  are  known, 
though  but  few  species  are  pathogenic;  these 
classes  are  (1)  the  sarcodinea  (ameboid), 
which  includes  the  Ameba  coli  of  dysentery 
(Fig.  10);  (2)  the  flagellata,  non-ameboid 
but  motile  by  means  of  flagella;  (3)  the 
sporozoa  living  within  the  bodies  of  other 
animals,  a  class  which  includes  the  hemo- 
sporidia,  ameboid  motile  parasites  living 
in  the  blood,  and  of  which  the  malarial 
germs,  Plasmodium  malaria?  (quartan  fever, 
seventy-two-hour  cycle),  the  Plasmodium 
prfecox     (estivo-autumnal     fever,      twenty- 


1  The  terms  mycetozoa  and  protozoa  seem  to  he  practically  synonymous  to  path- 
ologists, who  use  the  term  protozoa  in  the  sense  of  mycetozoa  as  above  defined. 
(36) 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE     37 

four  or  forty-eight-hoiir  cycle,  Fig.  11),  the  (\ytorrliyctes  variohe 
sen  vacciiifie  (the  probable  cause  for  smallpox  and  chickenpox)  are 
examples;  (4)  the  infusoria. 


Fig.  7 


Fig.  S 


Penicillium  with  spores.     (Mycomycetes, 
non-pathogenic.)     (Lehmann.) 


a,  saccharomyces;    h,  cell  with  four 
spores.      (Lehmann.) 


Fig.  9 


Fig.  10 


1,  ameba  from  dysenteric 
stool,  with    vacuoles  and  in- 
closed   red    cells;    2,    ameba 
from  straw  infusion:     3,    the 
Saccharomyces    (oidium)    albicans.      (After  Grawitz,     same       encysted.       X       600. 
in  Lehmann.)  (Kiinster.) 


38     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

Some  of  the  protozoa  act   by   entrance  to  the  intestinal  tract  as 
Ameba  coh  of  dysentery;  some  by  direct  contact  of   the  healthy 


Fig.   U 


Plasmodium  praecox  (forty-eight  hours).  Cycles  of  estivo-autumnal  parasite  1, 
very  young  form;  2,  infection  of  one  cell  with  seven  young  parasites  (drawn  from  a 
marrow  smear);  3,  triple  infection,  two  parasites  joined  by  single  chromatin  mass; 
4,  double  infection,  peculiar  rings  with  two  chromatin  grains  at  opposite  poles;  5, 
double  infection,  small  ring  adherent  to  cell;  6,  7,  signet  ring  forms,  subdivision  of 
chromatin;  8,  9,  later  ring  forms,  with  subdivided  chromatin  and  few  pigment  grains; 
10  to  12,  full-grown  forms,  with  finely  subdivided  chromatin  and  gradual  concentra- 
tion of  pigment;  13,  14,  stages  of  presegmenting  forms,  with  concentrated  eccentric 
pigment;  15,  double  infection,  with  separate  presegmenting  bodies;  16,  estivo- 
autumnal  rosette;  17,  18,  young  crescent  and  ovoid;  19,  "pulsating"  crescent; 
20  to  22,  various  forms  of  crescents;  23,  two  bows  about  single  crescent;  24,  fully 
developed  crescent,  two  masses  of  chromatin,  achromatic  substance,  double  wreaths 
of  pigment;  25,  diagrammatic  flagellating  body;  26,  extracellular  sterile  body. 
(Schmaus  and  Ewing.) 

with  the  diseased  surface  or  the  infected  object,  as  Treponema 
pallidum  of  syphilis  (not  yet  positively  classed  with  the  protozoa) 
or  Trepanosoma  equiperdum  of  equine  syphilis  (Dourine).     Some 


MICROORGyiNISMS  AS  EXCITING  CAUSES  OF  DISEASE      39 

act  only  through  an  intermediary  host  as  in  the  case  of  the  pUis- 
modia  of  malaria  through  the  anopheles  mosquito.  For  a  more 
extensive  description  of  the  action  of  protozoa,  see  works  on  general 
pathology. 

Fig.  12 


^N^-- 


a,  spiral  forms  with  a  flagellum  at  only  one  end;  b,  bacillus  of  typhoid  fever  with 
fiagella  given  off  from  all  sides;  c,  large  spirals  from  stagnant  water  with  wisps  of 
flagella  at  their  ends  (Spirillum  undula).     (Abbott.) 

The  vegetable  fungi  are  divided  into  (1)  Basidiomycetes,  which 
form  spores  borne  upon  basidia.  The  Achorion  schonleinii,  cause 
of  tinea  favosa  or  favus,  a  disease  of  the  hair,  usually  of  the  head, 
is  an  example.  (2)  Mycomycetes  (common  molds)  many-celled, 
characterized  by  mycelium.  Form  sporangia,  conidia,  and  asci. 
Example:  Oidium  albicans,  cause  of  thrush  and  aphthous  ulcer, 
frequently  in  the  mouth.  Trichophyton  tonsurans,  cause  of  barbers' 
itch.  (3)  Phycomycetes  (mucor  molds).  Resemble  algse,  but 
destitute  of  chlorophyl;  occasionally  pathogenic  in  man.  (4)  Sach- 
aromycetes  (Blastomycetes),  yeasts.  Useful  in  vinous  and  bread 
fermentation;  occasionally  causes  a  vegetative  dermatitis  called 
cutaneous  blastomycosis.^  (5)  Schizomycetes,  or  bacteria.  Being 
without  chlorophyl  (the  green  coloring  matter  of  plants  which 
synthesizes  CO2  and  water  into  starch),  the  fungi  are  unable  to  utilize 
the  simple  compounds,  such  as  carbon  dioxid  and  ammonia,  as  foods, 
and  are  therefore  compelled  to  break  down  the  complex  organic 
compounds,  for  which  purpose  they  are  competent  by  reason  of  their 
enzymes.  All  classes  of  fungi  have  representatives  which  produce 
disease  in  the  human  body,  but  the  schizomycetes  furnish  by  far 
the  greater  number  of  infectious  disease  causes. 

Chemically,  bacteria  are  about  85  per  cent,  water,  together  with 
albumin,  called  mycoprotein,  ferments,  soluble  extractives,  salts, 
sometimes  nuclein  bases,  coloring  matters,  organic  acids,  sulphur, 
starch,  and  cellulose. 

The  schizomycetes  (Greek  schizo,  to  split,  and  mukes,  a  fungus) 
are  minute  single-celled  plants  without  nuclei,  but  possessed  of  a 

1  See  Hyde  and  Montgomery,  Diseases  of  the   Skin. 


40     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

cell  wall  and  cell  protoplasm  (mycoprotein).  They  have  a  size  of 
about  1  micron  (1m=  2^F(T¥or  inch)  or  less  in  their  smallest  diameter. 
Some  of  them  possess  flagella,  hair-like  processes,  often  very  numer- 
ous, arising  from  the  protoplasm  rather  than  the  wall,  with  which 

Fig.   13 


Typhoid  bacilli  stained  by  Van  Ermengem's  method  to  show  flagella. 

they  lash  the  fluid  surrounding  them,  and  by  which  means  they 
effect  locomotion  (Fig.  12).  Other  bacteria  again  are  non-motile. 
Entering  the  organic  compounds,  carbohydrates,  hydrocarbons,  and 
nitrogenus  (albuminous)  substances,  they  ferment  or  decompose 
them,   forming  new  products,   and  extract  from  them  substances 


Fig.  14 


oo 


\ 


c  d  e 

a,  staphylococci;    h,  streptococci;    c,  diplococci;   d,  tetrads;   e,  sarcinae.      (Abbott.) 

necessary  to  their  growth  and  subsequent  reproduction.  The  sub- 
stance in  which  they  thus  grow  is  called  the  medium  or  soil.  The 
conditions  under  which  this  is  accomplished  are:  (1)  The  fungi  must 
have  a  proper  vitality.     (2)  Their  food-supply  or  soil  must  be  suited 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE     41 

to  their  growth  and  must  be  moist.  When  dried  tlie,y  may  retain 
their  vitahty  without  development  for  months.  In  general  terms 
the}^  require  water,  CNO,  and  salts.  (3)  The  temperature  must  be 
suitable;  they  grow  more  actively  at  about  102°  F.;  at  160°  F. 
maintained  they  usually  die,  but  in  some  cases,  as  with  the  typhoid 
bacilli,  they  may  live  in  the  spore  form  at 
even  212°  F.  or  over  unless  maintained  for  ^^^-  ^^ 

some  time.    Some  that  develop  best  at  high  ;<> -^ir  ^"^->i-  _: 

temperature  are  called  thermophilic.    Low  ~>^^--^'^5^^"'c■lX• 

temperature,  as  32°  F.  or  far  below  that,       ''i^^^<p^'^Yz^''^Z^^^^ 
inhibits  their  growth,  but  does  not  neces-       'J'/^^'^^^',l'^'<:''/7' 
sarily  kill  them.     (4)  Their  waste  products       ""  ''..*'    :::-j' 

must  be  removed  or  they  die  in  them.  Zooglea  of  bacilli.  (Abbott.) 
This  is  said   to   be  due  to  the  reaction, 

whether  acid  or  alkaline,  and  not  to  any  of  the  other  by-products — 
e.  g.,  in  lactic  fermentation  2  per  cent,  of  lactic  acid  is  about  the 
greatest  amount  endured  by  them.  They  are  also  sensitive  to  and 
inhibited  by  agitation,  daylight,  electric  light,  and  electric  currents. 
Morphologically  the  schizomycetes  are  grouped  into  several  families 
according  to  form,  methods  of  reproduction,  and  motion.  The 
following  is  Migula's  classification  modified  by  McFarland:^ 

I.  Family  Coccacese. — Cells  globular,  becoming  slightly  elongate 
before  division,  which  takes  place  in  one,  two,  or  three  directions 
of  space.    Formation  of  endospores  very  rare. 

1.  Streptococcus. — Division  in  one  direction  of  space  only,  producing 
chains  of  organisms  like  strings  of  beads.    No  flagella. 

2.  Micrococcus. — Division  in  two  directions  of  space,  so  that  fours 
or  tetrads  are  often  formed.    No  flagella. 

3.  Sarcina. — Division  in  all  three  directions  of  space.  Leading 
to  the  formation  of  bale-like  packages  of  cocci.     No  flagella. 

4.  Planococcus. — Division  in  two  directions  of  space,  like  micro- 
coccus.   Flagellated. 

5.  Planosarcina. — Division  in  three  directions  of  space,  and  like 
sarcina,  but  provided  with  flagella. 

IL  Family  Bacteriaceae. — Cells  more  or  less  elongate,  cylindric,  and 
straight.  Never  form  spiral  windings.  Division  in  one  direction 
of  space  only,  transverse  to  the  long  axis. 

1.  Bacterium. — Without  flagella.    Occasional  endospores. 

2.  Bacillus. — Flagella  arising  from  all  parts  of  the  surface.  Endo- 
sporulation  usual. 

3.  Pseudomonas. — Flagella  attached  only  at  the  ends  of  the  cells. 
Endosporulation  rare. 

1  Text-book  of  Pathology. 


42     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

III.  Family  Spirillacese. — Cells  spirally  twisted  like  a  corkscrew,  or 
short  and  curved  and  representing  segments  of  the  spiral.  Division 
transverse  to  the  long  diameter. 

1.  Spirosoma. — Rigid.    Without  flagella. 

2.  Microspira. — Rigid.  One,  two,  or  three  undulating  flagella 
attached  to  the  ends. 

3.  Spirillum. — Rigid.  From  five  to  twenty  semicircular  or  undu- 
lating flagella  attached  to  the  ends. 

4.  Spirocheta. — Serpentine  and  flexile.  Flagella  not  observed. 
Movement  probably  accomplished  by  means  of  an  undulating  mem- 
brane. 

IV.  Family  Mycobacteriaceae. — Cells  forming  more  or  less  elon- 
gate, cylindric  filaments,  often  clavate-cuneate  or  irregular  in  form. 
No  endospores,  but  formation  of  gonidia-like  bodies  due  to  segmen- 
tation of  the  cells.  No  flagella.  Division  transverse  to  the  long 
diameter.     Not  surrounded  by  a  sheath  as  in  chamydobacteriacese. 

1.  Mycobacterium. — Cells  in  their  usual  form,  short  cylindric 
rods,  often  bent  and  irregularly  cuneate.  At  times  Y-shaped  forms 
or  longer  filaments  with  true  branchings.  Sometimes  produce 
short  coccoid  elements,  perhaps  gonidia.  (This  genus  includes  the 
corynebacterium  of  Lehmann-Neumann.) 

2.  Actinomyces. — Cells  in  their  ordinary  form  occur  as  long 
branched  filaments.  Produce  gonidia-like  bodies.  Cultures  usually 
have  a  moldy  appearance,  due  to  the  development  of  aerial  hyphse. 

V.  Family  Chamydobacteriacese. — ^Vary  in  different  stages  of 
their  development.  Characterized  by  a  surrounding  sheath  about 
both  branched  and  unbranched  threads.  Division  transverse  to 
the  length  of  the  filaments. 

1.  Cladothrix. — Characterized  by  pseudo-dichotomous  branchings. 
Division  only  transverse.  Multiplication  by  the  liberation  of  whole 
branches.  Transplantation  by  means  of  flagellated  swarm  spores 
which  are  actively  motile. 

2.  Crenothrix. — Cells  united  in  unbranched  threads,  which  in 
the  beginning  divide  transversely  only.  Later  the  cells  divide  in 
all  three  directions  of  space.  The  products  of  final  division  become 
spherical  and  serve  as  reproductive  elements. 

3.  Pharagmidiothrix.— Cells  at  first  united  into  unbranched 
threads.  Division  in  all  three  directions  of  space.  Late  in  develop- 
ment, by  the  growth  of  certain  cells  through  the  delicate,  closely 
approximated  sheath,  branched  forms  are  produced. 

4.  Thiothrix. — Unbranched  cells  inclosed  in  a  delicate  sheath. 
Non-motile.  Division  in  one  direction  of  space.  Cells  contain  sulphur 
grains. 


MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE     43 

VI.  Family  Beggiatoacese. — Cells  united  to  form  tlireads,  whieh 
are  not  surrounded  by  an  inclosing  sheath.  The  septa  are  scarcely 
visible.  Division  transversely  only.  Motility  accomplished  through 
an  undulating  membrane. 

Beggiatoa. — Cells  contain  sulphur  grains. 


Fig.  16 

(I     tl~    >'^    -^ 


"/         .<>       ^/f 


a  b  c  d 

a,  Bacillus  subtilis  with  spores;   6,  Bacillus  anthracis  with  spores;   c,  Clostridium  with 
spores;   d,  bacillus  of  tetanus  with  end  spores. 

If  in  division  the  micrococci  agglomerate  like  a  bunch  of  grapes, 
without  a  definite  arrangement  in  pairs,  etc.,  they  are  called  often 
staphylococci  (staphle,  a  grape).  During  reproduction  bacteria 
may  excrete  a  material  which  unites  them  into  a  gelatinous  mass 
called  zooglea.  Some,  as  the  pneumococcus,  form  a  gelatinous  capsule 
about  themselves,  the  office  of  which  is  not  known. 


Fig.  17 

a  b 

a,  spirillum  of  Asiatic  cholera  (comma  bacillus) ;    b,  involution  forms  of  this  organism 
as  seen  in  old  cultures.     (Abbott.) 

The  bacilli  in  the  course  of  reproduction  may, form  long  threads, 
showing,  as  a  rule,  the  traces  of  segmentation.  Under  certain  un- 
favorable conditions  of  development  a  bacillus  forms  a  glistening 
oval  body  within  itself  (endospore)  which  resists  stains.  The  body  of 
the  bacillus  may  attenuate  into  a  capsule  for  the  spore.  When  the 
spore  germinates  this  bursts  open  and  the  new  bacillus  escapes. 
These  spores  are  very  resistant  to  devitalizing  agents.  The  bacilli - 
forming  spores  are  said  to  be  in  the  resting  stage.  These  spores 
under  favorable  conditions  again  form  bacilli  like  their  progenitors, 
but  do  not  form  other  spores  without  this  return  to  the  bacillus  form. 
A  single  cell  forms,  as  a  rule,  but  one  spore. 

If  the  entire  bacterium  is  changed  into  the  spore  form  they  are 
called  arthrospores;  when  cocci  take  on  the  appearance  of  spores 


44     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

they  are  also  called  arthrospores.  Under  unfavorable  conditions 
bacteria  may  undergo  degeneration  and  take  on  abnormal  or  involu- 
tion forms,  and  when  the  conditions  are  again  favorable  to  develop- 
ment they  may  resume  their  typical  forms. ^  While  these  form 
changes  occur,  bacteria  are  never  permanently  changed  from  one 
form  to  another.^  Those  bacteria  which  have  several  forms  in  their 
life  cycle  are  termed  pleomorphic.  Those  having  but  one  form  are 
monomorphic.  Ptomains  are  products  of  decomposition  of  the 
medium  and  some  are  poisonous  if  taken  in  as  food.  Those  bacteria 
which  exist  on  living  tissue  are  known  as  parasitic.  They  enter  the 
body  by  way  of  open  wounds  or  surfaces  deprived  of  epithelium, 
or  may  lodge  at  certain  points  of  the  mucous  surface  of  the  lungs, 
skin  openings,  or  the  alimentary  canal.  If  not  killed  out  they  multiply 
in  the  natural  juices  of  the  part  on  which  they  locate  and  produce  an 
infective  inflammation.  Poisonous  substances  may  be  generated, 
which  are  absorbed  into  the  system  and  may  act  as  poisons,  pro- 
ducing toxemia.  When  the  toxin  is  soluble,  diffuses  from  the  bacteria 
and  floats  in  the  blood  it  is  called  extracellular  toxin  or  exotoxin; 
when  confined  to  the  bacteria  and  Hberated  upon  dissolution  of  the 
bacteria,  it  is  called  endotoxin;  when  the  free  toxin  gives  the  reaction 
for  albumin  it  is  called  a  toxalbumin. 

The  character  of  both  the  inflammation  and  the  poisoning  depends 
upon  the  particular  bacterium  or  bacteria  present.  The  bacteria 
may  in  certain  cases  be  taken  into  the  blood,  and,  coming  to  rest  at 
certain  spots,  the  above-described  process  is  repeated. 

The  Bacillus  anthracis  divides  in  the  blood  stream,^  and  other 
organisms,  such  as  the  Bacterium  pneumoniae  and  Bacillus  influenzae 
and  the  pyogenic  organisms  may  exist  in  it.  They  ma}^  thus  localize 
in  a  spot  and  produce  effects.  This  has  some  significance  in  the 
production  of  blind  apical  abscesses  and  pericemental  abscess  (dental) 
and  in  the  reverse  general  infection  from  dental  sources.  Many 
forms  of  organisms  exhibit  a  preference  for  certain  spots  at  which 
they  find  the  conditions  best  suited  to  development — e.  g.,  the  typhoid 
bacillus  in  the  glands  of  the  ileum,  Peyer's  patches;  the  anthrax 
bacillus  in  the  lungs  of  animals;  the  diphtheria  bacillus  in  the 
mucous  surfaces  of  the  pharynx  and  contiguous  parts.  Bacteria 
may  enter  the  blood  via  the  mucosa  of  the  alimentary  canal,  but 
this  is  ordinarily  highly  resistant.  Those  parasitic  bacteria  which 
produce  disease  are  called  pathogenic,  others  are  non-pathogenic. 

1  Abbott,  Principles  of  Bacteriology. 

-  The  subject  of  transmutation  when  certain  bacteria  (as  Streptococcus  viridans)  are 
gradually  changed  from  anaerobic  to  aerobic  conditions  is  now  under  study. 
3  Green,  Pathology  and  Morbid  Anatomy. 


FERMENTATION  45 

The  mouth  offers  a  suitable  habitat  for  many  bacteria. 

The  bacteria  which  hve  on  dead  organic  matter  are  called  sapro- 
phytic (sapros,  rotten,  and  phidon,  a  plant).  They  break  up  the 
dead  animal  and  vegetable  matter  into  simple  compounds  like 
carbon  dioxid,  ammonia,  etc.,  which  are  utilized  by  the  higher  chlor- 
ophyllous  plants.  The  nitrogen  of  the  air  is  also  utilized  by  some 
plant  bacteria,  and  can  be  introduced  to  aid  crops.  As  animals  are 
dependent  upon  plants  for  existence,  their  vast  importance  in  the 
economy  of  nature  is  evident.  Bacteria  may  often  pass  from  a  para- 
sitic existence  to  a  saprophytic  one — a  fact  which  is  utilized  in  their 
study  by  bacteriologists,  who  prepare  artificial  media  in  which  to 
cultivate  them.  These  are  called  cultures,  which  by  transference  from 
one  culture  plate  to  another  of  like  kind  are  said  to  be  passed  through 
generations.  When  by  careful  segregation  one  form  of  bacterium  is 
separated  from  others  present  in  a  mixed  culture  and  thereafter 
cultivated  alone,  it  is  called  a  pure  culture;  when  the  bacteria  are 
thinly  spread  on  a  gelatin  or  agar  culture  and  then  isolated,  the 
grouped  bacteria  developing  at  each  point  are  called  a  colony. 
Bacteria  may  pass  from  a  saprophytic  to  the  parasitic  form  of  exist- 
ence. Bacteria  which  have  this  power  of  adaptation  to  a  new  form 
of  medium  are  called  facultative.  When  without  this  power,  they 
are  obligate  bacteria. 

According  to  Pasteur,  those  which  develop  in  the  presence  of  free 
oxygen  as  in  the  air  are  called  aerobic.  Those  which  cannot  live 
in  its  presence  are  anaerobic.  These  derive  the  necessary  oxygen 
from  'the  medium.  Those  which  live  either  way  are  facultative. 
Those  compelled  to  either  mode  of  existence  are  obligate. 

When  bacteria  produce  pigment  either  within  themselves  or  their 
medium,  they  are  termed  chromogenic;  when  they  produce  light  or 
phosphorescence,  they  are  termed  photogenic.  If  they  have  the 
ability  to  produce  fermentation,  they  are  termed  zymogenic;  when 
they  produce  gas  they  are  called  aerogenic. 

FERMENTATION. 

Fermentation  in  the  broadest  acceptation  of  the  term  has  been 
defined  as  the  decomposition  of  substances  possessing  complex 
molecules  under  the  influence  of  organized  (living)  or  unorganized 
ferments  (enzymes).  The  decompositions  occur  when  organic  sub- 
stances are  exposed  to  the  action  of  fungi  or  their  enzymes,  or  are 
subjected  to  the  action  of  certain  ferments  such  as  are  found  in  the 
digestive  fluids  secreted  into  the  elimentary  canal,  which  are  really 
enzymes  also  derived  from  living  cells. 


46     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

According  to  Woodhead/  the  molecules  of  the  fermented  compound 
are  separated  from  one  another  for  a  brief  period  and  then  allowed  to 
combine  and  form  simpler  and  more  stable  compounds.  The  process 
is  accompanied  by  heat  due  to  chemical  changes. 

Ferments,  then,  are  of  two  kinds:  (1)  organized  or  formed  fer- 
ments or  living  fungi  which  multiply  at  the  expense  of  the  sub- 
stance which  they  are  fermenting;  (2)  unorganized  or  unformed 
ferments  or  enzymes,  nitrogenous  bodies  produced  by  living  cells 
which  have  the  power  of  producing  chemical  changes  in  organic 
substances.  They  thus  affect  many  times  their  own  weight  of  the 
particular  organic  substance  being  fermented  without  being  them- 
selves much  affected,  though  eventually  exhausted  (catalysis). 
Typical  examples  are  the  pepsin  of  the  gastric  juice,  which  changes 
albumin  to  peptone,  and  the  ferment  of  the  yeast  plant,  proved 
capable  of  changing  sugar  into  alcohol  and  carbon  dioxid,  even 
when  the  cells  themselves  are  crushed  and  filtered  out. 

The  unorganized  ferments  usually  act  by  oxidizing,  deoxidizing, 
or  hydrating  the  substance  modified.  They  act  best  when  their 
products  are  removed  from  the  neighborhood. 

Many  bacteria  have  been  shown  to  possess  such  unorganized  fer- 
ments. It  is  probable  that  they  produce  their  effects  on  organic 
substances  by  the  aid  of  these  ferments,  which  serve  them  as  pepsin 
serves  man  (extracellular  ferments).  It  is  thought  that  in  other 
cases  the  germs  take  up  organic  food,  digest  it,  and  excrete  waste 
products  in  somewhat  the  same  manner  that  the  body  cells  nourish 
themselves  by  intracellular  ferments  (p.  23).  As  a  rule,  more  than 
one  species  of  bacterium  infects  a  fermentable  substance.  The 
more  active  varieties  predominate  in  the  fermentation,  but  mixed 
fermentations  may  proceed.  In  some  cases  the  bacterial  multipli- 
cation is  favored  by  the  activity  of  other  bacteria  (symbiosis),  in  some 
cases  the  development  is  retarded.  Some  may  die  out,  finding  an 
unfavorable  soil.  After  a  time  the  predominating  bacteria  may  die 
in  the  waste  products  accumulated  about  them,  leaving  the  field 
clear  for  a  second  or  third  variety.  In  this  way  progressive  decom- 
positions may  occur — e.  g.,  the  alcoholic  fermentation  may  be  suc- 
ceeded by  the  acetic,  in  which  the  alcohol  is  changed  to  acetic  acid, 
as  in  cider- vinegar  formation.  The  nature  of  the  chemical  changes 
produced  in  a  fermentable  substance  depends  upon  the  chemical 
nature  of  the  medium  and  upon  the  nature  of  the  fungus  causing  the 
fermentation. 

Thus,  in  an  infusion  of  vegetable  juices  containing  sugar  a  yeast 

'  Bacteria  and  their  Products. 


FERMENTATION  47 

fungus  (one  of  the  blastomycetes)  will  produce  carbon  dioxid  gas 
and  alcohol  if  the  oxygen  of  the  air  be  freely  admitted  (aerobiosis), 
while  if  to  a  fresh  portion  of  the  same  solution  scrapings  from  carious 
dentin  be  added,  lactic  acid  will  be  formed,  and,  as  a  rule,  no  gas. 
Moreover,  the  reaction  will  occur  if  oxygen  be  excluded  (anaero- 
biosis).  In  albuminous  compounds  an  alkaline  reaction  and  entirely 
different  substances  will  be  formed  upon  the  addition  of  carious 
dentin.  Probably  upon  this  fact  depend  the  different  effects  of 
bacterial  plaques  upon  the  teeth.     (See  Caries  and  Pyorrhea.) 

The  ferments  or  enzymes  produced  by  bacteria  are  quite  numerous. 

Proteolytic  ferments  dissolve  albuminous  substances;  proceed 
under  an  alkaline  reaction  and  sometimes  under  an  acid  reaction. 

Diastatic  ferments  change  starch  into  sugar.     (See  Dental  Caries.) 

Inverting  enzymes  convert  saccharose  into  dextrose  or  non- 
fermentable  forms  of  sugar  to  fermentable  ones.  (See  Dental 
Caries.) 

Coagulating  ferments  coagulate  milk.  Coagulation  is  also  pro- 
duced in  the  tissues  and  exudate  in  inflammation  by  the  ferments 
of  pyogenic  micrococci. 

Siigar-splitting  ferments  change  sugar  into  other  products,  as 
alcohol,  carbon  dioxid,  and  lactic  acid. 

Fat-sjjJitting  ferments  split  fats  into  glycerin  and  fatty  acids. 

Hydrolytic  ferments  cause  a  combination  with  the  elements  of . 
water  in  substances  they  decompose. 

Emulsifying,  oxidizing,  and  nitrif^dng  ferments  also  occur. 

Toxins  are  also  classed  with  the  ferments,  and  are  capable  of 
producing  new  substances  when  distributed  in  the  blood.  (See 
Immunity.) 

Putrefaction. — The  progressive  decomposition  of  albuminous 
matter  into  simple  compounds  is  effected  by  many  bacteria  through 
processes  of  oxidation,  deoxidation,  and  hj^dration. 

Peptones^  are  first  formed,  next  alkaloid-like  bodies  called  pto- 
mains  (putrefactive  alkaloids);  succeeding  this  such  nitrogenous 
bases  as  leucin,  tyrosin,  and  the  amins  (methyl,  ethyl,  and  propyl- 
amin)  are  formed;  next  fatty  acids  and  such  acids  as  butyric,  lactic, 
and  succinic  acid  appear;  next  aromatic  products  such  as  indol, 
phenol,  and  cresol  are  formed,  and  the  final  decomposition  is  repre- 
sented in  the  end  products — carbon  dioxid,  CO2;  hydrogen  sulphid, 
H2S;  ammonia,  NH3;  and  water,  H2O.  When  bacteria  produce 
decomposition  of  living  animal  tissue  they  effect  this  putrefaction 
as  distinctly  noted  in  certain  cases  of  abscess. 

1  Ziegler,  General  Pathologj\ 


48     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

Such  products  of  bacterial  action,  either  produced  in  a  Hving  or 
a  saprophytic  medium,  as  are  capable  of  acting  as  poisons  in  the 
animal  organism  are  called  toxins.  Some  animal  parasites  also  pro- 
duce them.  It  is  understood  that  they  differ  according  to  the  fungus 
and  the  medium.  If  the  toxin  be  proteid  in  nature,  it  is  termed  a 
toxalbumin. 

Some  of  the  ptomains  are  toxic;  the  greater  number  are  not.  The 
poisoning  due  to  the  eating  of  putrefactive  meats,  fish,  etc.,  containing 
them  is  known  as  "ptomain  poisoning."'^ 


Fig.   18 


Fig.   19 


Staphylococcus  pyogenes  aureus 
(micrococcus).  From  a  culture.  X 
1000.      (Green.) 


Streptococcus  pyogenes.  From  pus 
found  in  a  pyemic  abscess.  X  1000. 
(Green.) 


When  the  toxins  alone  are  absorbed  from  a  focus  of  infection  the 
subject  is  poisoned — a  condition  called  toxemia,  whether  due  to  a 
toxic  ptomain,  as  in  the  case  of  Asiatic  cholera,  or  to  a  toxalbumin, 
as  in  the  case  of  diphtheria.  Such  toxemia  is  commonly  accompanied 
by  more  or  less  fever,  according  to  the  amount  taken  up.  When  the 
organisms  enter  th,e  circulation  and  multiply  in  the  blood,  or  at  least 
move  about  and  live  in  it,  to  be  carried  to  capillaries  in  which  they 
can  rest  and  multiply,  the  condition  is  termed  a  septicemia.^  In 
toxemia  and  septicemia  the  symptoms  depend  upon  the  nature  of  the 
organisms  and  their  products.  (See  page  148.)  Bacteria  are  found 
everywhere  and  exist  upon  the  surface  of  the  body,  in  its  external 
cavities,  and  in  the  alimentary  canal.  Here  under  conditions  of  health 
there  seem  to  be  conditions  favoring  certain  forms,  which,  when 
implanted,  occupy  the  field  and  exclude,  except  temporarily,  other 

1  For  a  table  of  origins,  formulae,  and  toxicity  of  ptomains,  see  Gould's  Medical 
Dictionary. 

2  Abbott,  Principles  of  Bacteriology. 


FERMENTATION  49 

forms  to  which  the  soil  is  not  so  well  suited.  These  are  known  as  the 
"normal  flora."  It  has  been  shown,  however,  that  the  growth  of 
some  bacteria  is  favored  by  the  presence  of  certain  others  (symbiosis) . 
This  is  said  to  be  characteristic  of  Vincent's  angina,  in  which  the 
fusiform  bacillus  is  symbiotic  with  a  spirochetal  form. 

After  certain  changes  occur  in  the  medium,  other  forms  may  become 
implanted.  Pathogenic  bacteria  may  exist  in  the  healthy  cavities 
and  produce  no  ill  results.  Again,  the  soil  may  favor  and  disease 
begins.  Certain  bacteria  have  been  found  constantly  present  in 
relation  with  certain  diseases — e.  g.,  the  spirillum  of  Asiatic  cholera 
with  that  disease,  the  Treponema  pallidum  with  syphilis;  these  are 
specific  bacteria.  Taken  from  individuals  with  the  disease,  they 
produce  it  in  susceptible  animals  inoculated  with  them  if  circum- 
stances favor  their  growth. 

Fig.  20 


Mouse's  lung;  vessels  plugged  with  Bacilli  anthracis:  a,  alveolus;  v,  vein  full  of  bacilli: 
c,  capillaries  also  full;   br,  bronchus.      X  400.     (Horsley.) 


Bacteria  spread  in  the  tissues  along  the  lines  of  least  resistance. 
They  may  follow  the  cellular  tissue  or  enter  the  l^^mphatics,  or  pass 
at  once  into  the  veins  and  be  carried  into  the  circulation.  They  may 
be  strictly  localized  at  the  point  of  infection. 

Thus  there  may  be  a  localized  inflammation — e.  g.,  in  simple 
abscess  due  to  the  Staphylococcus  pyogenes  aureus;  a  diffuse  inflam- 
mation, as  in  case  of  infection  by  the  Streptococcus  pyogenes.;  a 
gland  infection  or  a  septicemia,  as  in  anthrax  or  in  a  general  infection 
by  Streptococcus  pyogenes  or  Bacterium  pneumonise;  or  a  metas- 
tatic inflammation,  as  in  pyemia,  in  which  the  germs  (usually  Strepto- 
coccus pyogenes)  gain  access  to  the  blood  from  a  local  focus  of  infec- 
4 


50      MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

tion  and  are  carried  to  distant  parts,  in  which  they  cause  abscesses 
while  the  products  produce  toxemia.  To  produce  effect,  germs  in 
the  blood  must  come  to  rest  at  some  point,  which  may  occur  in 
the  capillaries  owing  to  their  injury,  in  thrombi  or  emboli,  or,  in  case 
of  entrance  of  bacteria  into  a  leukocyte,  they  may  migrate  into  the 
connective  tissue  (Fig.  20). 

It  has  been  shown  that  pyogenic  germs  may  exist  in  the  blood 
without  local  effects,  while  again  a  local  injury  may  cause  the  arrest 
of  the  germs  and  a  secondary  local  inflammation  or  abscess  be  set 
up.  This  is  due  to  simple  arrest  or  to  extravasation  of  blood,  which 
permits  the  germs  to  pass  from  the  vessels  into  the  connective  tissue. 

General  or  local  depression  of  tissue  vitality  acts  as  a  predisponent 
to  local  infection. 

The  infections  themselves  are  classified  as  primary,  secondary, 
and  mixed. 

The  primary  is  the  original  infection,  say,  e.  g.,  Bacillus  tubercu- 
losis. The  secondary  is  that  implanted  when  the  original  disease  is 
well  under  way — e.  g.,  Streptococcus  pyogenes  aureus  upon  tuber- 
culosis; a  third  or  tertiary  infection  is  possible.^ 

The  original  infection  may  be  by  mixed  germs,  more  than  one  of 
which  may  multiply.  Thus,  the  Streptococcus  pyogenes  aureus  and 
Bacterium  pneumoniae  may  both  be  found  in  an  abscess.  This  is  a 
mixed  infection. 

BACTERIA   OF   THE   MOUTH. 

In  even  the  best-cared-for  mouths  bacteria  are  numerous  and  find 
the  conditions  suited  to  their  growth.  In  unclean  mouths  containing 
food  debris,  dead  epithelium,  etc.,  their  life  conditions  are  much 
more  favorable. 

According  to  Miller^  there  are  a  number  of  bacteria  which  invari- 
ably occur  in  every  mouth.    These  are: 

1.  Leptothrix  innominata. 

2.  Bacillus  buccalis  maximus. 

3.  Leptothrix  buccalis  maxima. 

4.  Jodococcus  vaginatus. 

5.  Spirillum  sputigenum. 

6.  Spirochete  dentium  (denticola). 
To  this  list  Goadby^  has  added: 

Leptothrix  racemosa  of  Vicentini,  further  described  by  Williams.^ 

1  Park,  Surgery  by  American  Authors. 

2  Microorganisms  of  the  Human  Mouth. 

3  Mycology  of  the  Mouth,  1903. 

4  Dental  Cosmos,  1899.     See  Dental  Caries. 


BACTERIA  OF  THE  MOUTH 


51 


Fig.  21 


Streptothrix  buccalis. 

Streptococcus  brevis  of  Lingelsheim  and  Cladothrix  buccalis  (pro- 
visionally added.) 

With  the  exception  of  Streptococcus  brevis  and  perhaps  Clado- 
thrix and  Bacillus  buccalis  maximus,  these  have  been  until  recently 
uncultivable  on  laboratory  media,  and  are  strictly  obligate  parasites. 
Of  the  last-named  organism,  Goadby  obtained  biological  character- 
istics of  the  pure  culture,  but  he  did  not  establish  its  disease-producing 
power,  if  it  possesses  any.  Noguchi,^  working  in  the  Rockefeller 
laboratories,  has  cultivated  several 
forms  of  oral  treponemata  (so-called 
spirocheta)  by  the  use  of  ascitic  fluid 
and  fresh  sterile  tissue  in  the  medium. 
(See  Pyorrhea  Alveolaris) . 

Certain  pathogenic  organisms 
have  been  shown  to  be  present  in 
the  mouths  of  healthy  persons, 
such  as  bacteriological  investigators; 
those  nursing  infectious  diseases, 
such  as  diphtheria,  scarlet  fever, 
etc.,  and  even  in  the  mouths  of 
healthy  individuals  apparently  not 
exposed  to  any  infection.  In 
about  10  per  cent,  of  all  individuals 
examined  at  random,  Netter  found 
Staphylococcus  pyogenes  aureus 
(golden  pus) .  Staphylococcus  pyo- 
genes albus  was  also  found.    The 

Pneumococcus,  or  Bacterium  pneumoniae,  was  found  in  the  mouths 
of  about  15  per  cent,  of  healthy  individuals.  This  organism  has  been 
found  by  Kirk  to  be  apparently  causative  of  pericemental  abscess, 
and  has  been  reported  by  Schreier^  as  found  in  75  per  cent,  of  cases 
of  apical  abscess  examined.  It  has  also  been  related  with  cases  of 
osteomyelitis  and  Ludwig's  angina.  The  Bacillus  diphtheriee  of 
Loffler  has  been  found  in  about  10  per  cent,  of  mouths  examined 
at  random,  and  33  per  cent,  of  600  children  in  a  school  examined 
during  an  epidemic  of  diphtheria  were  found  to  have  the  bacillus 
present  in  the  mouth,  while  but  about  2  per  cent,  developed  the 
disease.^  This  latter  fact  shows  the  absolute  necessity  for  at  least 
a  local  predisposition  as  well  as  an  exciting  cause. 


Diplo cocci  pneumonise  entangled  in 
the  meshes  of  the  fibrinous  exudation. 
From  a  section  of  lung  in  the  "red 
hepatization"  stage  of  acute  pneu- 
monia. In  the  upper  part  of  the  field 
is  a  cell  containing  several  cocci — 
possibly  a  phagocyte.  X  1000. 
(Green.) 


1  Journal  of  Experimental  Medicine,  vol.  xv. 
^  Goadby. 


2  Dental  Cosmos,  1893. 


52     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

The  Bacillus  tuberculosis  exists  in  the  mouths  of  many  suffering 
from  pulmonary  tuberculosis,  and  exists  also  at  times  in  the  mouths 
of  the  healthy.  The  Saccharomyces  albicans  may  be  present  and 
at  times  produce  thrush  (Fig.  9). 

Fig.  22 


Bacillus  diphtherise :   A,  its  morphology  on  glycerin-agar-agar;   B,  its  morphology  on 
Loffler's  blood  serum;   C,  its  morphology  on  acid  blood-sei-um  mixture.     (Abbott.) 


The  Bacillus  typhosus  (typhoid)  has  been  found  in  the  healthy 
mouth,  and  at  times  has  oral  pathogenicity.  Many  other  organisms 
have  been  isolated  from  the  human  mouth.  Some  of  these  have  a 
specific  character,  of  others  little  is  known.  The  mouths  of  pro- 
fessional nurses  have  been  shown  to  contain  bacteria,  which  increased 
the  danger  of  infection  of  their  patients,  and  that  the  sanitation  of 
their  mouths  reduced  the  danger.  Some  of  the  bacteria  of  the  mouth 
possess  the  power,  under  certain  conditions,  of  felting  themselves 
in  plaques  upon  the  surfaces  of  the  teeth.  Here,  if  properly  supplied 
with  carbohydrate  food,  some  of  them  produce  lactic  acid  and 
decalcify  the  teeth.  Some  bacteria  have  a  later  putrefactive  action 
upon  the  organic  matrix  of  the  dentin.  Some  of  the  masses  may 
develop  an  alkaline  reaction  due  to  putrefaction.  Goadby^  gives 
an  interesting  classification  of  bacteria  found  in  dental  caries  (which 
see).  Some  bacteria  not  yet  isolated  are  the  probable  causes  of 
pyorrhea  alveolaris.    (See  chapter  on  Pyorrhea  Alveolaris).     M.   T. 


1  Mycology  of  the  Mouth. 


THE  RESISTANCE  OF  THE  TISSUES  TO  INFECTION        53 

Barrett^  has  discovered  an  ameba  constantly  associated  with  pyor- 
rhea alveolaris.     (See  P^^orrhea  Alveolaris.) 

The  bacteria  in  the  mouth  probably  are  taken  into  the  food  and 
swallowed  in  great  numbers.    Many  are  doubtless  killed  by  the  gas- 
tric juice,  which  is  a  weak  germicide;  notwithstanding,  some  pyo- 
genic cocci  and  some  of  the  blastomycetes  may  develop  in  the  stomach 
and  produce  disease.    Many  also  may  enter  the  intestines  and  either 
excite  disease   of  specific   character   or  pro- 
duce abnormal  intestinal  fermentations,  the  ^^^-  ^"^ 
toxins  of  which  may  be  absorbed,  and  pro-                ^        i^fe,  <»>»,„^^ 
duce   malnutritional   conditions.    They  may         v  '^1^' 
remain  localized  in  the  mouth  and  produce                '      ,'*""5-^ 
oral  disease,  dental   caries,  or  pericemental           I  / 
diseases,  etc.;  abscesses,  pyorrheas,  etc.,  are       v.        t^k      ' 
unquestionably  the  causes  in  many  instances             .     ^^      \. 
of  fever,  septic  infection,  intestinal  disturb-               / 
ances,   endocarditis,  pulmonary  tuberculosis,      ^    .„        ,       , 

,        ,    ,  ,  .    .         .    „  .  Bacillus  tuberculosis.      X 

glandular  enlargements,  ]omt  miiammations  looo.    (Green.) 

of  rheumatic  character,   skin  eruptions,  etc. 

The  relation  of  an  unclean  mouth  to  effects  upon  the  mouth,  ali- 
mentary canal  and  air  passages  and  blood  and  lymph  channels,  is, 
therefore,  a  direct  one  of  an  importance  that  renders  exact  studies  in 
this  direction  of  extreme  value.  The  saliva,  while  not  germicidal 
(Miller),  may  or  may  not  contain  substances  acting  as  pabulum  for 
the  growth  of  bacteria,  but  probably  does  in  many  cases  apart  from 
extraneous  food  materials  introduced.  It  has  been  considered  by 
Hugenschmidt  that  the  saliva  is  positively  chemotactic,  attracting 
many  leukocytes  to  the  oral  mucous  membrane;  also  the  great 
vascularity  of  the  part  probably  aids  in  reducing  effective  inoculation. 

THE   RESISTANCE    OF    THE    TISSUES    TO   INFECTION. 

The  resistance  of  the  tissues  to  bacteria  is  to  be  considered  from 
two  main  standpoints:  (1)  The  prevention  of  the  entrance  of  bac- 
teria into  the  tissues.  (2)  The  destruction  of  the  bacteria  after 
entrance  into  the  tissues. 

1.  The  prevention  of  entrance.  It  has  been  shown  that  pathogenic 
bacteria  may  enter  the  mouth,  alimentary  canal,  lungs,  etc.,  but  few 
develop. 

The  skin  acts  as  a  mechanical  barrier,  though  its  openings  may  at 
times  harbor  bacteria. 

The  mucous  membrane  secretes  mucus,  which  envelops  bacteria 

1  Paper  read  before  the  Pennsylvania  State  Dental  Society  and  the  National  Dental 
Association,  1914.     (See  Dental  Cosmos,  August,  1913.) 


54     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 


and  with  it  they  are  carried  away.     The  healthy  mucus  also  has 
apparently  a  devitalizing  power  for  some  bacteria,  not  for  others. 


Fig.  24 


/'  2 

1,  a  spore  which  has  penetrated  the  intestinal  wail  and  entered  the  abdomina 
cavity,  where  four  leukocytes  have  surrounded  its  end:  m,  the  muscular  layer  of  the 
intestine;  e,  epithelial  layer;  s,  the  serous  layer.  2,  a  spore  surrounded  by  leuko- 
cytes from  the  abdominal  cavity  of  a  Daphne.     (Metchnikoff.) 

The  acid  gastric  juice  kills  many,  but  some  may  pass  through,  two 
or  three  hours  after  a  meal,  at  times  when  the  gastric  juice  is  not 

active.    Probably  the  intestinal 
Fig.  25  juices  also  inhibit,  in  large  de- 

gree, the  action  of  such  as  have 
entered  the  alimentary  canal. 
In  all  cases  the  agitation  of  the 
fluids  of  a  part  seems  to  act 
mechanically  to  prevent  locali- 
zation of  bacteria. 

2.  The  prevention  of  develop- 
ment in  the  tissues.  Within  the 
healthy  tissues  bacteria  find 
several  elements  opposing  their 
development. 

It  seems  the  consensus  of 
opinion  among  pathologists  that 
the  blood  serum  normally  con- 
tains germicidal  substances 
probably  of  the  nature  of  a 
nuclein  and  called  by  Buchner 
"alexins." 

This  belief  is  mainly  based 
upon  the  demonstration  of  Nut- 
tall  that  filtered  blood  serum  pos- 
sesses the  power  of  producing  the 
degeneration  of  bacteria.  Buchner  found  that  heating  to  55°  C. 
destroyed  this  property,  a  fact  pointing  to  the  albuminous  nature  of 
the  alexins.  After  reviewing  all  the  evidence,  Vaughan  and  Novy^ 
conclude: 

'  Cellular  Toxins. 


Active  phagocytosis.  Endothelial  cells 
enclosing  the  bacilli  of  swine  septicemia, 
from  an  hepatic  vein  of  a  pigeon:  a,  a, 
indothelial  cells;  b,  b,  leukocytes. 
(Metchnikoff.) 


THE  RESISTANCE  OF  THE  TISSUES  TO  INFECTION        55 

"  (1)  the  exact  nature  of  the  germicidal  constituents  of  the  blood  or 
alexins  is  not  known;  (2)  the  alexins  have  their  origin  in  the  white 
blood  corpuscles;  (3)  disintegration  of  the  white  blood  corpuscles 
liberates  alexins;  (4)  it  is  probably  true  that  alexins  are  also  secreted 
by  living  leukocytes."  Authorities  disagree,  some  claiming  multi- 
plicity of  alexins,  others  that  only  one  alexin  exists  in  a  given  serum 
(Metchnikoff). 

Metchnikoff,  in  1884,  demonstrated  that  the  leukocytes  take 
up  bacteria  within  themselves  and  claimed  that  they  thus  destroy 
them.  This  process  he  termed  phagocytosis  (phago,  I  eat;  cytos, 
a  bud).  The  polymorphonuclear  leukocytes,  called  microphages 
by  Metchnikoff,  and  the  large  mononuclear  leukocytes,  which  he 
called  macrophages,  have  this  power.  The  macrophages  take  up 
dead  leukocytes.  It  is  now  considered  that  this  property,  which 
is  also  possessed  by  the  endothelial  cells  of  the  bloodvessels  and 
serous  cavities,  is  but  evidence  of  the  nutritive  function  of  simple 
cells  occurring  after  the  bacteria  have  been  partially  degenerated 
by  the  serum  (Fig.  25).  This  is  borne  out  by  experiments:  Mixed 
pyogenic  cocci  and  leukocytes  free  from  blood  serum  exhibiting  no 
phagocytic  activity,  whereas  when  the  bacteria  are  first  exposed  to 
blood  serum  and  then  to  phagocytes,  there  is  marked  phagocytosis. 
(See  Opsonins.)  In  some  cases  bacterial  disintegration  may  liberate 
the  intracellular  toxins  and  thus  permit  the  toxic  effects  upon  the 
host.  This  is  said  to  be  true  in  case  of  administration  of  typhoid 
vaccines  during  the  course  of  the  actual  disease. 

Researches  of  Leber,  Buchner,  and  others  have  shown  that  leuko- 
cytes may  be  attracted  by  certain  bacterial  products  even  in  high 
dilution,  and  by  other  chemical  substances  such  as  mercury  and 
copper  salts.  This  is  called  positive  chemotaxis.  The  opposite  is 
negative  chemotaxis.  It  has  been  shown  that  the  negative  may  be 
followed  by  marked  positive  chemotaxis. 

Toxins  are  negatively  chemotactic,  and  when  bacteria  produce 
much  toxin  phagocytosis  and  suppuration  are  lessened,^  e.  g.,  in 
s'treptococcus  infection.  Many  other  bacterial  products  and  bac- 
terial proteins  are  positively  chemotactic,  and  when  they  are  pro- 
duced in  place  of  much  toxin  phagocytosis  is  increased,  and  the 
bacteria,  if  few,  are  coincidently  destroyed  by  the  alexins  and  taken 
up  by  the  phagocytes  with  resolution,  or,  if  the  bacteria  be  numerous, 
suppuration  is  increased  and  the  bacteria  expehed  as  a  protection 
to  the  body.  It  has  been  shown,  however,  that  the  taking  up  of 
living  bacteria  may  occur  and  may  spread  an  infection.    Also  it  has 

1  Stengel,  A  Text-book  of  Pathology. 


56      MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

been  shown  that  the  microphages  take  up  some  bacteria  and  the 
macrophages  take  up  others. 

If  the  combined  local  forces  be  incompetent  to  kill  out  the  infecting 
organisms,  the  local  infection  spreads  until  limited  or  the  patient 
dies;  or  a  metastasis  may  occur,  in  which  case  the  process  is  prac- 
tically repeated  in  another  locality. 

IMMUNITY. 

Immunity  is  the  opposite  of  predisposition,  or  susceptibility, 
and  may  be  defined  as  that  condition  of  the  local  fluids,  the  blood, 
or  the  body  cells,  in  which  inoculation  with  bacteria  or  bacterial 
products  has  no  injurious  effects. 

There  is  also  some  relative  immunity  to  non-infectious  diseases, 
e.  g.,  females  to  hemorrhagic  diathesis.  (See  Predisposition  p.  30.) 
Immunity  to  infective  agencies  may  be  natural  or  acquired. 

Natural  Immunity. — This  is  due  to  a  healthy  action  of  the  phago- 
cyte of  the  body  or  to  some  peculiar  substance  in  the  blood;  the 
antibody  of  the  particular  bacterium,  or  fungus  or  toxin  which  it 
is  thought  may  be  inherited  from  ancestors. 

Typical  examples  of  this  kind  of  immunity  are  those  of  the  rat  to 
dphtheria;  man  to  rinderpest;  lower  animals  to  syphilis;  the  negro 
to  yellow  fever  (though  he  is  susceptible  to  smallpox);  the  hog  to 
snake  venom,  etc. 

Natural  immunity  may  change  to  susceptibility  through  some 
change  in  the  systemic  condition.  Thus,  two  students  attending  a 
scarlet-fever  ward  for  months  became  susceptible  through  the  effects 
of  a  long  walk  and  hunger;  both  took  the  fever,  one  dying.^ 

Rats,  run  in  a  wheel  until  exhausted,  were  successfully  inoculated 
with  anthrax  bacilli,  to  which  they  are  normally  insusceptible.  These 
states  of  tissue  fatigue  are  noted  in  the  overstrain  of  athletes,  who 
often  suffer  from  furuncle.  According  to  Gildersleeve^  examination 
shows  that  the  opsonic  index  is  greatly  lowered  by  the  overstrain. 
Metchnikoff  considers  immunity  due  to  an  enzyme  derived  from  the 
leukocytes  called  microcytase,  which  either  acts  within  the  leuko- 
cytes or  outside  of  them  to  produce  deterioration  of  the  bacteria 
(cytolysis),  and  that  it  may  require  other  factors  to  act  with  it  as 
amboceptor  or  complement. 

Natural  immunity  may  therefore  fail  upon  severe  test,  and 
survival  of  the  test  is  the  only  certain  assurance.  This  natural 
immunity  may  be  of  two  kinds: 

1  Green,  Pathology  and  Morbid  Anatomy.  ^  Lecture. 


IMMUNITY  i)i 

1.  Natural  toxin  immunity,  e.  g.,  hog  to  snake  venom. 

2.  Natural  bacterial  immunity,  e.  g.,  negro  to  yellow  fever. 
Acquired  Immunity. — This  is  of  two  kinds : 

1.  Acquired  toxin  immunity. 

2.  Acquired  bacterial  immunity. 

Acquired  Toxin  Immunity. — Toxin  immunity  may  be  acquired  in 
two  ways: 

1.  By  the  injection  of  small  doses  of  toxins  at  intervals  until  no 
reaction  results.  The  horse  is  so  immunized  in  diphtheria  antitoxin 
production.    The  antitoxin  is  produced  by  the  cells  of  the  horse. 

2,  By  the  injection  into  man  or  animals  of  serum  containing  anti- 
toxin produced  by  method  No.  1.  The  former  is  an  active  immunity; 
the  latter  passive. 

Acquired  Bacterial  Immunity. — Immunity  to  bacterial  inoculation 
may  be  acquired  in  several  ways : 

1.  Naturally,  through  having  had  an  attack  of  the  particular 
specific  disease;  thus,  as  a  rule,  measles,  smallpox,  syphilis,  yehow 
fever,  and  many  other  infectious  diseases  cause  the  body  cells  to 
produce  substances  antagonistic  to  the  bacteria  known  as  anti- 
bodies which  are  said  to  be  in  part  the  cause  of  immunity.  Phago- 
cytosis is  increased  against  subsequent  infections  which  remain  in 
the  blood  and  render  the  individual  immune  to  a  second  attack, 
though  in  some  cases  this  immunity  is  lost. 

2.  Artificially,  through  the  injection  into  the  body  of  attenuated 
bacteria,  cultivated  through  several  generations  under  unfavorable 
conditions;  for  example,  at  increased  temperatures  or  in  the  presence 
of  weak  antiseptics  or  by  passing  them  through  other  animals, 
whereby  their  virulence  is  lost;  a  mild  immunizing  attack  ensues. 
Thus  in  rabies,  or,  rather,  for  prevention  of  rabies,  after  the  bite 
of  an  animal  suffering  from  it,  accurately  graduated  doses  of  emul- 
sions of  the  spinal  cord  of  infected  rabbits,  dried  for  varying  periods 
to  produce  accurately  degenerated  rabies  germs,  are  injected  into 
man,  preventing  the  development  of  the  germs  introduced  by  the 
bite.  The  emulsion  of  older  cords  are  injected  first,  then  those  of 
younger  cords  (dried  for  a  shorter  time) .  The  use  of  cowpox  vaccine 
against  smallpox  is  of  this  nature. 

3.  Artificially,  by  the  injection  of  dead  bacteria  from  a  pure  culture 
of  the  specific  bacterium  from  which  immunity  is  sought.  (Wright's 
vaccine.)  What  is  known  as  the  opsonic  index  is  raised,  and  the 
person  becomes  more  resistant  to  that  particular  infection;  that  is 
to  say,  phagocytosis  is  increased.     (See  Opsonins.) 

4.  Artificially,  by  the  injection  of  graduated  doses  of  toxins,  pro- 
duced in  a  saprophytic  medium  by  the  specific  bacterium,  all  bacteria 


58     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

being  filtered  out.  This  is  most  readily  done  when  the  toxins  pro- 
duced lie  in  the  medium  external  to  the  bacteria  (extracellular  toxins) . 
The  horse  is  so  treated  in  the  production  of  diphtheria  antitoxin  for 
use  in  the  diphtheria  of  man. 

5.  Artificially,  by  the  injection  of  the  serum  of  animals  immunized 
by  method  No.  4,  which  serum  contains  a  substance  antagonistic  to 
the  specific  toxin  and  known  as  an  antitoxin.  Thus  the  injection 
of  horse  serum  containing  antitoxin  of  diphtheria  produced  by 
method  No.  4  into  a  diphtheric  patient  aborts  the  disease  by  antago- 
nizing its  toxin  while  the  phagocytes  kill  out  the  bacteria.  Injection 
into  the  attending  nurse  produces  immunity  to  the  disease,  but 
antitoxin  does  not  act  upon  the  bacteria  but  upon  the  toxin.  The 
immunity  then  is  probably  due  to  phagocytosis  and  an  amboceptor 
which  aids  it. 


Fig.  26 


Fig.  27 


C— 


A,  complement;  B,  ambo- 
ceptor; C,  receptor;  D,  part 
of  cell.  Showing  how  comple- 
ment destroys  bacteria  through 
the  agency  of  amboceptors. 


Cell  with  different  kinds  of  receptors:  C, 
receptors.  The  dark  objects  represent  food 
molecules,  toxins,  etc. 


The  methods  1,  2,  3,  and  4  produce  a  much  more  lasting  immunity, 
as  the  antagonizing  substance  is  the  result  of  cell  reaction  on  the 
part  of  the  individual,  and  is  called  active  immunity;  that  produced 
by  method  No.  5  is  passive  immunity,  because  not  produced  by 
cell  reaction,  but  directly  introduced  into  the  blood,  and  is  much 
less  lasting.     It  is  not  effective  for  all  bacteria. 

The  various  forms  of  acquired  immunity  are  explainable  by  the 
now  generally  accepted  theory  of  Ehrlich  known  as  the  side-chain 
theory. 


IMMUNITY  59 

Ehrlich's  Side-chain  Theory. — This  theory  is  based  upon  certain 
demonstrated  facts  and  upon  the  supposition  that  each  cell  is  com- 
posed of  aggregations  or  groups  of  atoms  and  surrounded  by  side 
groups  of  atoms  (molecules),  which  compose  the  cell  protoplasm. 
Each  atom  group  is  supposed  to  have  its  own  chemical  affinity  for 
food  elements,  poisons,  etc.,  as  shown  by  the  selective  affinity  of 
drugs. 

These  chemical  atom  groups,  therefore,  have  a  receptive  function 
and  are  called  receptors  on  the  cell.  Other  groups  have  a  fermenta- 
tive action  and  chemically  change  the  substances  presented;  these 
are  called  zymoyhorous  atom  groups. 

Each  toxin  molecule  has  an  afiinity  for  some  cell  receptors,  other- 
wise no  effect  is  produced  by  it.  (Snake  venom  has  no  effect  upon 
the  hog.) 

The  receptor  is  considered  to  possess  a  group  of  atoms  suited  to  a 
prehending  action,  whereby  it  combines  with  the  toxin  molecule  (or 
food  molecule  in  nutrition),  which  possesses  a  similar  combining 
group  of  atoms.  In  each  th^se  are  termed  the  haptophorous  group. 
The  toxin  molecule  is  capable  of  inflicting  injury  upon  or  stimulating 
cell  action,  as  shown  in  the  case  of  tetanus,  in  which  tonic  muscular 
contractions  are  excited.  The  group  of  atoms  in  the  toxin  mole- 
cule which  accomplishes  this  is  termed  the  toxophorous  group 
(Fig.  27). 

That  the  body  cells  neutralize  the  toxin  if  not  in  overwhelming 
quantity  is  shown  by  the  experiment  of  Wassermann  and  Takaki, 
in  which  a  mixture  of  brain  emulsion  and  tetanus  toxin  was  inert 
when  injected  into  a  susceptible  animal.  Therefore,  a  zymophorous 
group  of  atoms  is  said  to  exist  in  the  cell  or  its  receptor. 

The  Theory  of  Toxin  Immunity. — The  toxin  produced  during  an 
infective  disease,  such  as  diphtheria,  and  floating  in  the  blood, 
presents  itself  to  cells  for  some  receptors  of  which  it  has  an  affinity. 
The  haptophorous  atom  group  of  its  molecules  joins  with  the  hapto- 
phorous atom  group  of  the  receptor.  The  toxophorous  atom  of  the 
toxin  group  exerts  its  action  upon  the  receptor  and  is  neutralized  by 
the  zymophorous  group  of  the  latter  unless  the  toxin  is  in  too  great 
quantity.  The  cell,  in  case  of  injury,  repairs  itself  by  forming  an 
excess  of  the  particular  kind  of  receptors  having  afiinity  for  the  partic- 
ular toxin.  These  receptors  become  detached  and  float  in  the  blood, 
and  there  have  the  same  affinity  for  the  toxin.  These  are  called 
receptors  in  the  blood,  and  constitute  what  is  known  as  antitoxin. 
They  are  known  to  be  formed  by  the  body  cells  and  not  by  the  blood, 
as  they  have  been  found  in  the  tissue  juices  of  blood-making  organs 
immediately  after  the  introduction  of  toxin,  while  at  the  same  time 


60     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 


not  found  in  the  blood,  though  they  afterward  appear,  as  might  be 
expected  (Fig.  28). 

The  antitoxin  receptor  (with  affinity  for  the  toxin  molecule)  has 
an  haptophorous  atom  group  which  combines  with  the  haptophorous 
group  of  the  toxin  molecule,  which,  having  found  its  affinity  in  the 
blood,  is  satisfied,  does  not  further  affect  the  cells  proper,  and  thus 
cell  injury  is  prevented.  This  occurs  naturally  in  each  case  of 
diphtheria,  and  probably  recovery  or  death  is  dependent  upon  the 
ability  of  the  body  cells  to  furnish  (1)  antitoxin  sufficient  to  antagonize 
the  toxin  and  (2)  another  body  to  be  described  which  antagonizes  the 
bacteria. 

Fig.  28  Fig.  29 


Showing  separation  of  antitoxins,  and 
combinations  of  toxins  (dark)  with  free  anti- 
toxins in  the  blood. 


Showing  the  action  of  anti- 
complement:  A,  complement;  B, 
intermediary  body;  C,  receptor; 
D,  cell;   E,  anticomplement. 


In  the  case  of  diphtheria-serum  therapeutics,  the  horse  is  com- 
pelled by  method  No.  4  to  form  these  antagonizing  substances,  and 
the  serum  is  then  injected  into  the  individual  suffering  an  attack 
or  threatened,  thus  furnishing  him  ready  made  the  antagonizing 
substances  (antitoxin,  etc.).  A  special  antitoxin  is  supposed  to  be 
formed  for  each  kind  of  toxin.  Ehrlich  believes  an  antitoxin  mole- 
cule to  be  capable  of  satisfying  200  toxin  molecules,  and  that  they 
combine  chemically.  In  old  sera  the  toxin  undergoes  a  chemical 
change  into  toxoid,  and  the  injection  of  this  causes  an  increase  of 
receptors  on  the  cell,  and  thus  renders  the  animal  more  susceptible 
to  the  action  of  the  toxin.  An  antitoxin  unit  is  the  amount  of 
antitoxin  necessary  to  neutralize  an  arbitrary  amount  of  a  particular 
toxin. 


IMMUNITY  61 

Toxon  is  a  third  body  produced  by  the  bacteria  which  has  some 
affinity  for  antitoxin,  but  the  combination  is  still  somewhat  toxic 
(has  a  different  toxophorous  group  of  atoms),  and  in  diphtheria  is 
credited  with  the  production  of  postdiphtheric  paralysis.  The 
attempt  to  make  antitoxins  has  not  been  successful  in  most  cases. 

The  Theory  of  Acquired  Bacterial  Immunity. — ^When  bacteria  enter 
the  tissue  of  an  animal  by  inoculation  and  are  not  destroyed  by  the 
alexins  and  phagocytes,  they  develop  and  produce  toxins  and  may 
themselves  enter  the  blood.  A  reaction  of  the  body  cells  occurs,  as 
shown  by  fever,  and  not  only  antitoxin,  but  a  new  body  is  pro- 
duced by  the  cells,  which,  with  the  aid  of  still  another  substance 
called  complement,  is  capable  of  destroying  the  particular  bacterium 
causing  the  infection.  This  body  is  another  form  of  receptor  having 
two  haptophorous  groups,  by  which  it  links  the  complement  with 
the  receptor  of  the  bacterium,  and  thus  enables  the  complement  to 
destroy  the  bacterium  through  its  zymophorous  atom  group.  The 
doubly  haptophorous  receptor  is  called  from  this  fact  the  amboceptor 
(also  intermediary  or  immune  body)  (Fig.  26).  A  different  ambo- 
ceptor is  produced  for  each  bacterium  and  the  host  is  immunized 
against  this  bacterium  only.    ' 

The  complement,  of  which  there  are  several  in  association  in  the 
blood  (Ehrlich),  is  probably  produced  by  the  leukocytes,  and  is 
classed  among  the  alexins.  As  stated,  it  has  a  zymophorous  atom 
group,  and  also  has  an  haptophorous  atom  group  with  which  it 
joins  the  amboceptor.  The  complement  is  destroyed  at  55°  C.  (is 
thermolabile).  The  amboceptor  requires  a  higher  heat  (is  thermo- 
stabile) . 

In  natural  bacterial  immunity  it  is  thought  that  some  of  the 
amboceptors  are  inherited  from  immune  ancestors,  and  that  they 
exist  together  with  complement  in  the  blood  ready  to  act.  Metchni- 
koff  claims  that  amboceptor  and  complement  are  products  of  the 
leukocytes.  The  elements  in  blood  serum  which  destroy  bacteria 
are  termed  hacteriolysins,  and  the  new  bodies  formed  by  cells  as  a 
protection  are  called  antibodies. 

Agglutination. — -When  body  cells  react  to  infection,  and  attempt  to 
or  effect  immunity,  the  blood  plasma  may  acquire  the  property  of 
clumping  the  bacteria  together,  and  they  settle  to  the  bottom  of  a 
test  serum,  leaving  the  fluid  clear.  It  is  supposed  to  be  exliibited 
only  toward  the  bacterium  causing  the  infection,  but  experimentally 
out  of  the  body  (in  vitro)  others  are  sometimes  affected. 

The  substance  producing  agglutination,  called  agglutinin,  evi- 
dently exists  in  blood  as  the  result  of  cell  reaction.  It  is  of  the 
nature  of  liberated  amboceptors,  but  has  a  zymophorous  group.    It 


62     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

therefore  acts  by  combining  by  an  haptophorous  group  and  acting 
through  a  zymophorous  group. 

The  reaction  is  useful  in  making  an  early  diagnosis  of  the  kind  of 
existing  infection.  Thus  if  typhoid  bacillus  be  suspected  as  a  cause 
of  disease  present  and  be  the  cause,  the  blood  serum  drawn  from  the 
patient  will  agglutinate  living  typhoid  bacilli  placed  in  it.  This  is 
known  as  Widal's  reaction. 

Precipitins. — A  substance  of  nature  and  origin  similar  to  agglutinin 
causes  precipitation  instead  of  agglutination.  It  is  used  in  diagnosis 
and  in  differentiating  the  blood  of  animals,  a  matter  of  importance 
in  murder  cases. 

Opsonins. — Wright  found  that  when  bacteria  were  mixed  with 
leukocytes  in  the  absence  of  serum  phogocytosis  did  not  occur,  but 
if  serum  was  then  introduced  it  did  occur.  Also  if  leukocytes  were 
washed  with  sodium  citrate-chlorid  solution  to  free  them  from  serum, 
and  bacteria  that  had  been  previously  treated  with  serum  were 
introduced,  phagocytosis  occurred.  Obviously,  then,  the  serum  con- 
tains a  substance  or  substances  capable  of  favoring  phagocytosis. 

It  is  regarded  that  this  substance  prepares  the  bacteria  for  the 
phagocytic  process,  and  from  this  fact  Wright  named  these  sub- 
stances opsonins,  which  are  therefore  classed  among  the  alexins. 
Opsonins  have  an  haptophorous  group  of  atoms  prehending  the  bac- 
teria and  a  zymophorous  group  acting  upon  them.  Other  observers 
have  determined  that  opsonins  are  multiple  in  normal  blood.  The 
degree  of  activity  of  the  opsonin  related  to  a  particular  infection  when 
compared  with  that  of  a  healthy  person  is  called  the  opsonic  index. 

The  Opsonic  Index. — To  test  the  opsonic  index,  an  even 
emulsion  of  the  bacteria,  the  serum  of  the  infected  patient,  the 
serum  from  each  of  several  healthy  persons,  and  healthy  leukocytes 
from  the  healthy  persons  are  necessary. 

1.  The  Emulsion. — The  pure  culture  is  isolated.  A  2  per  cent, 
nutrient  agar  medium  has  sterile  milk,  milk  serum,  or  blood  serum 
added  in  the  proportion  of  1  part  to  3  of  the  nutrient  agar.  In 
tubes  of  the  selected  medium  slant  cultures  are  made,  and  incubated 
at  37.5°  C.  for  eighteen  to  twenty-four  hours.  (Gildersleeve.)  These 
are  then  washed  from  the  surface  of  the  medium  with  0.85  per  cent, 
sodium  chlorid  solution  and  the  solution  placed  in  a  sterile  bottle 
with  sterile  glass  beads  or  sand  and  shaken  to  remove  clumps. 
The  number  of  bacteria  in  each  cubic  centimeter  is  then  estimated 
(standardized)  and  a  dilution  made  on  the  basis  of  this  estimated 
count  with  0.85  per  cent,  sodium  chlorid  solution,  so  that  when 
opsonized  with  normal  serum  each  leukocyte  will  take  up  from  5  ta 
8  of  ordinary  bacteria.     (Gildersleeve.) 


IMMUNITY  63 

2.  The  Sera. — These  are  obtained  from  the  patient  and  healthy 
persons  by  congesting  the  finger  with  a  rubber  band  and  bleeding 
into  a  capsule  or  pipette,  which  is  then  sealed  and  the  blood  allowed 
to  clot  in  the  incubator  for  15  to  20  minutes. 

The  leukocytes  are  obtained  by  filling  with  blood  a  centrifuge 
tube,  three-fourths  full  of  a  1  per  cent,  solution  of  sodium  citrate 
in  0.85  per  cent,  solution  of  sodium  chlorid.  After  shaking,  the 
tubes  are  centrifugalized,  the  fluid  drawn  from  the  buffy  coat,  and 
the  latter  then  carefully  pipetted  and  drawn  in  and  out  to  mix 
thoroughly. 

The  preparations  being  ready,  equal  volumes  of  bacterial  emulsion, 
the  serum  to  be  tested,  and  leukocytes  are  drawn  into  a  marked 
pipette,  each  volume  being  separated  by  a  bubble  of  air.  These 
are  then  mixed  by  drawing  in  and  out,  and  the  end  of  the  pipette  is 
sealed  and  the  pipette  placed  in  an  opsonizer  for  fifteen  or  twenty 
minutes.  The  pipette  end  is  then  broken,  and  the  contents  spread 
evenly  on  several  glass  slides  by  means  of  another  slide.  (Gilder- 
sleeve.) 

These  are  then  air  dried  and  stained.  The  bacteria  in  a  given 
number  of  leukocytes  are  counted  and  the  total  divided  by  the 
number  of  leukocytes  counted,  thus  obtaining  the  average  of  bac- 
terial ingestion  per  leukocyte.  This  gives  the  phagocyting  index  for 
the  infected  individual. 

The  same  procedure  exactly  is  carried  out  with  the  normal  sera, 
and  the  average  phagocyting  index  determined.  The  index  is  cal- 
culated by  dividing  the  patient's  phagocyting  index  by  the  normal 
phagocyting  index,  or  the  same  thing  may  be  done  by  the  following 
proportion : 

Normal  index  :  patient's  index  ::  1  :  x. 

If  X  is  above  1,  the  patient's  index  is  high. 

If  X  is  below  1,  the  patient's  index  is  low  or  subnormal. 

Vaccine  Therapy. — Wright  found  that  when  a  large  number  of  the 
bacteria  causing  the  infection  were  killed  and  then  injected  into  the 
patient,  their  bodies  contained  substances  which  produced  a  cell 
reaction  resulting  in  an  increase  of  opsonin  and  phagocyting  power 
in  the  leukocyte  of  the  individual — this  determined  by  the  opsonic 
index. 

For  a  time — twenty-four  or  forty-eight  hours — the  index  became 
lower.  This  Wright  called  the  negative  phase;  afterward  it  gradually 
rose  to  a  maximum.  This  stage  he  termed  the  positive  phase.  The 
object  sought,  then,  is  to  increase  the  resistive  power  of  the  patient 
to  the  infection  through  an  increase  in  the  phagocytosis. 


64     MICROORGANISMS  AS  EXCITING  CAUSES  OF  DISEASE 

The  Vaccine. — This  is  prepared  by  producing  an  emulsion  of  the 
pure  culture  as  for  the  opsonic  index.  The  emulsion  is  then  stand- 
ardized by  an  estimation  of  the  bacteria  in  each  cubic  centimeter. 
The  bacteria  are  then  killed  by  heating  the  sealed  container  in  a 
water  bath  and  are  then  diluted  with  0.85  sodium  chlorid  solution 
(with  0.2  per  cent,  of  tricresol  or  phenol  added)  to  the  desired 
strength. 

The  proper  number  of  bacteria  for  one  maximum  dose  should  be 
contained  in  1  c.c.  of  the  diluted  emulsion.  To  determine  the  dilu- 
tion the  estimation  in  1  c.c.  of  standardized  emulsion  is  divided  by  the 
number  desired  as  a  dose,  and  the  quotient  less  1  equals  the  number 
of  c.c.  of  the  diluting  solution  to  be  added  to  1  c.c.  of  the  emulsion. 

The  Injection. — The  hypodermic  syringe  is  sterilized  and  filled 
with  the  diluted  emulsion  and  an  injection  made  into  a  convenient 
site,  which  should  be  previously  sterilized  with  2  per  cent,  phenol 
solution,  followed  by  sterile  water  and  absolute  alcohol  (Gildersleeve) . 
The  needle  should  be  inserted  into  the  subcutaneous  tissue  of  the 
outer  side  of  the  arm,  or,  if  preferred,  of  the  leg  or  thigh,  or  below 
the  angle-  of  the  scapula,  whichever  would  prove  most  convenient  for 
the  purpose. 

Gildersleeve^  recommends  smaller  doses  when  the  index  is  low,  in 
general  infection,  in  acute  conditions,  in  children,  and  in  individuals 
markedly  depressed,  than  in  the  opposite  conditions.  He  gives  the 
following  dosage  of  the  various  vaccines  employed  in  treating 
infections  of  the  oral  cavity: 

Micrococcus  aureus  and  albus 50,000,000  to  600,000,000 

Streptococcus  pyogenes 10,000,000  to  100,000,000 

Pneumococcus 10,000,000  to  100,000,000 

Micrococcus  catarrhalis 25,000,000  to  100,000,000 

Influenza  baciUus 25,000,000  to  100,000,000 

The  Reaction  of  the  Blood. — According  to  Michaels^  (following 
Gautrelet),  individuals  in  whom  the  oxidations  are  below  normal, 
and  w^ho  have  a  tendency  to  arthritic  diseases  because  of  an  excess 
of  the  acid  constituents  or  waste  products  in  the  body  fluids,  are 
denominated  hyperacid  individuals.  The  hyperacid  have  oxidations 
above  the  normal,  together  with  a  superabundance  of  saline  chlo- 
rids;  and  these  he  regards  as  more  subject  to  infection.  There  are 
three  ways  in  which  the  predisposition  of  the  hypoacid  might  be 
accounted  for: 


1  American  Text-book  of  Operative  Dentistry.     This  article  should  be  read  for  a 
more  extended  description. 

2  Sialosemiology. 


EXTERNAL  ANTIBACTERIAL  INFLUENCES  65 

1.  The  increased  amount  of  alkaline  elements  may  permit  an 
increased  alkalinity  of  the  blood,  rendering  it  favorable  to  bacteria 
as  a  culture  medium. 

2.  The  systemic  change  may  introduce  a  substance  into  the 
blood  which  is  a  suitable  pabulum  for  the  bacteria,  as,  for  example, 
excess  of  glucose  in  diabetes  (according  to  Kirk^  this  occurs  in  the 
saliva  in  those  susceptible  to  caries). 

3.  Certain  immunizing  substances,  opsonins,  alexins,  etc.,  may 
fail  to  be  formed. 

Per  contra,  the  hyperacid  may  be  immune  for  opposite  reasons. 
Whether  this  be  a  rational  explanation  or  not,  it  is  certainly  shown 
by  Wright  that  therapy  will  increase  the  opsonic  index,  and  it 
may  be  that  in  the  hyperacid  the  continuous  cell  irritation  by  the 
acid  elements,  as  CO.,,  uric  acid,  etc.,  may  cause  a  tissue  reaction 
increasing  alexin  or  opsonic  power. 

The  foregoing  is  merely  a  synopsis  of  the  main  facts  governing 
immunity.  There  are  many  details  which  are  omitted  and  for 
which  the  reader  is  referred  to  works  on  bacteriology. 

EXTERNAL  ANTIBACTERIAL  INFLUENCES. 

Many  chemical  substances  and  physical  forces  prevent  the  growth 
and  reproduction  of  bacteria  without  necessarily  killing  them;  these 
are  called  antiseptics;  a  weak  solution  of  boric  acid  is  an  example, 
agitation  is  another,  dryness  another.  Low  temperatures  also  pre- 
vent fermentation.  Other  substances  or  forces  kill  the  bacteria  after 
an  exposure  to  their  influence  for  a  sufficient  length  of  time;  these 
are  germicides — e.  g.,  a  1  to  1000  solution  of  mercuric  chlorid  in 
water,  boiling  water,  or  streaming  steam;  sunlight  for  some  bacteria. 
Other  substances  destroy  both  the  bacteria  and  their  products;  these 
are  disinfectants — e.  g.,  sodium  dioxid  or  other  substances  liberating 
nascent  oxygen.    Formaldehyde  and  iodin  are  also  disinfectant. 

1  Dental  Brief,  1907. 


CHAPTER   IV. 

DISTURBANCES  OF  NUTRITION. 

DisOKDERS  of  nutrition  are  of  three  classes:  (1)  due  to  an  excess 
of  nutritive  material  of  all  classes,  or  of  one  class;  (2)  due  to  a 
deficiency  of  nutritive  material,  active  or  relative;  (3)  due  to  the 
presence  in  the  blood  of  material  which,  instead  of  serving  the 
purpose  of  metabolism,  disturbs  it;  (4)  an  inability  of  the  cells  to 
appropriate  a  proper  quantity  and  quality  of  food. 

EXCESS    OF   NUTRITION;   HYPERNUTRITION. 

An  excess  of  nutrition  may  be  either  general  or  local.  If  local, 
it  is  associated  with  an  overfulness  of  the  bloodvessels  (hyperemia). 
If  the  individual  possess  a  general  richness  of  blood,  he  is  said  to  be 
plethoric.  Sthenic  plethora  is  such  a  richness  associated  with  activity 
of  the  circulation  and  a  consequent  increase  of  the  vital  processes 
due  to  plentiful  cell  nutrition,  and  with  an  active  repair  of  even 
excessive  waste  of  cell  protoplasm. 

In  asthenic  plethora,  on  the  contrary,  the  individual  is  full-blooded, 
but  the  circulation  is  sluggish;  waste  products  are  probably  accumu- 
lated in  the  blood  and  the  vital  processes  are  sluggish  in  consequence. 
Instead  of  the  rich  color  and  active  movements  associated  with 
sthenic  plethora,  the  asthenic  have  a  purplish  appearance  and  the 
movements  are  more  labored. , 

Local  Hypernutrition. — An  increased  stimulation  of  the  nerves  of 
a  part  invites  more  blood  to  it,  which  within  certain  limits  increases 
the  nutrition  to  the  cells  of  the  part.  This  results  in  increased  irri- 
tability, contractility,  and  general  functional  activity  of  the  func- 
tionating cells.  If  this  be  maintained,  the  cells  grow  or  multiply,  or 
both,  and  the  part  is  enlarged  and  capable  of  an  increased  amount 
of  work. 

Stimulation  beyond  this  point  causes  irritation  or  overstimulation 
of  cells,  and  the  vital  processes  become  fretful;  incomplete  chemical 
changes  occur  in  the  cells,  and  the  functional  activity  is  disordered. 
The  cells  are  wearied,  and  if  the  overstimulation  be  continued 
paralysis  from  overwork  results. 
(66) 


EXCESS  OF  NUTRITION;  HYPERNUTRITION  67 

Hypertrophy. — Though  strictly  meaning  an  excess  of  nutrition, 
this  term  signifies  an  increase  in  the  size  of  a  part  as  the  result  of 
stimulation  and  destruction,  with  a  compensatory  rebuilding  of 
cell  material  in  excess  (a  cell  hyperplasia)  (Weigert^).  The  new 
growth  must  be  practically  normal  in  structure.  As  a  rule,  both  the 
size  (simple  hypertrophy)  and  the  number  of  the  cells  (numerical 
hypertrophy  or  hyperplasia)  are  increased.  The  caliber  of  the 
bloodvessels  is  increased  to  comply  with  the  stimulus  to  their 
controlling  nerves — the  vasomotors.  Hypertrophy  is  frequently 
exhibited  in  tissues  subjected  to  an  unusual  amount  of  work  short 
of  marked  fatigue.  An  increase  in  its  function  occurs;  its  capacity 
for  work  becomes  greater,  and  if  the  strong  stimulus  (mild  irritation) 
implied  be  continued  the  cells  increase  in  size  and  it  may  be  in  number, 
all  three  phases  of  the  expenditures  of  an  increase  of  vital  energy 
being  represented — functional,  nutritive,  and  reproductive.  If  the 
heart  be  subjected  to  an  increase  in  the  strain  ordinarily  brought 
upon  it,  an  increase  in  the  volume  of  the  muscular  fibers  follows, 
causing  hypertrophy  of  the  walls.  The  same  is  true  of  the  muscles 
of  the  gravid  uterus,  in  which  the  cells  increase  to  many  times  their 
normal  length.  When  one  organ,  as  a  kidney,  takes  up  alone  the 
work  usually  performed  by  two  it  increases  in  size  (hypertrophies). 
This  is  called  compensatory  hypertrophy.  It  may  occur  in  an  organ 
which  endeavors  to  supply  the  deficient  function  in  another  organ 
of  different  sort.  Hypertrophy  also  occurs  in  many  inflammatory 
conditions,  and  is  due  to  the  area  of  hyperemia  surrounding  every 
focus  of  inflammation.  Thus  the  epithelium  about  the  edges  of  an 
ulcer  may  thicken  or  new  bone  may  be  formed  about  an  area  of 
inflamed  bone  tissue  or  periosteum.  The  bone  tissue  may  become 
more  compact,  a  condition  termed  sclerosis  of  bone,  as  it  results 
in  the  formation  of  formed  (intercellular)  tissue  at  the  expense  of 
the  cellular  elements. 

The  removal  of  an  accustomed  resistance  often  produces  an  irri- 
tation resulting  in  mild  hyperemia,  and  thickening  or  hypertrophy 
results — e.  g.,  non-occlusion  of  teeth  frequently  produces  hyper- 
cementosis. 

A  form  of  cellular  hypertrophy  appears  to  occur  in  certain  leuko- 
cytes, resulting  in  the  formation  of  a  multinucleated  cell  or  "giant 
cell." 

Under  irritation  the  nucleus  subdivides,  but  the  cell  body  fails  of 
division,  and  instead  of  complete  reproduction  a  large  cell  with  many 
nuclei  is  formed  (Fig.  30).    These  giant  cells  appear  where  tissue  is 

1  See  Abbott's  Principles  of  Bacteriology,  p.  601,  for  an  amplification  of  this  idea. 


68 


DISTURBANCES  OF  NUTRITION 


to  be  removed,  as  in  the  case  of  aseptic  foreign  bodies  or  the  roots 
of  deciduous  or  even  of  permanent  teeth.  (See  Resorption  of 
Temporary  Teeth.)  An  hypertrophy  or  excessive  development  may 
occur  during  intra-uterine  hfe  and  is  spoken  of  as  congenital  hyper- 
trophy. A  low  grade  of  inflammation  may  lead  to  a  numerical 
hypertrophy,  as  in  the  case  of  hypertrophy  of  the  dental  pulp 
(which  see). 

Hyperplasia. — Hyperplasia,  sometimes  called  false  hypertrophy,  is 
an  increase  in  size  partly  due  to  an  increase  in  the  number  of  the 
cells,  though  the  individual  cells  may  be  smaller  than  normal.  It 
occurs  mostly  in  the  connective  tissues,  though  it  ordinarily  plays 
a  part  in  most  hypertrophies.  The  part  is  usually  asymmetrical. 
Examples:  elephantiasis  and  hyperplasia  of  the  dental  pulp. 

Fig.  30 


Dog's  hair  encapsulated  in  subcutaneous  tissue:  a,  hair;  b,  fibrous  tissue;  c,  pro- 
liferating granulation  tissue;  d,  giant  cells.  Preparation  hardened  in  alcohol,  stained 
with  Bismarck  brown,  and  mounted  in  Canada  balsam.      X  66.     (Ziegler.) 


Cyst  and  Tumor  Formation. — A  cyst  is  an  enlargement  contain- 
ing a  cavity  which  in  turn  contains  liquid,  gelatinous,  or  pultaceous 
material,  about  which  is  a  capsule  condensed  from  the  surrounding 
structures.  The  accumulation  of  the  fluid  or  semifluid  contents 
produces  the  enlargement  of  the  part  even  if  bony  (Fig.  31). 

They  differ  from  tumors  in  being  strictly  localized,  though  they 
may  be  large,  and  in  their  generally  benign  character,  though  tumors 
may  at  times  have  a  cystic  character. 

Cysts  may  be  formed  by  the  retention,  secretion,  or  extravasation 
of  fluid  in  several  ways:  (1)  By  the  retention  of  normal  secretion  of 
a  gland  owmg  to  the  obstruction  of  its  duct — e.  g.,  ranula.  These 
are  called  retention  cysts.  (2)  By  abnormal  secretion  into  ductless 
cavities — e.  g.,  bursa?  (exudation  c^'sts).  (3)  By  the  extravasation 
of  blood  into  a  ductless  cavity  (extravasation  cyst).  (4)  Indepen- 
dently in  tissue  as  a  result  of  mucoid  or  fatty  changes  or  liquefaction 
necrosis,  the  surrounding  tissue  becoming  condensed  into  a  capsule 
(liquefaction  or  colliquation  cysts) .    (5)  Independently  as  a  collection 


EXCESS  OF  NUTRrrrON;   HYPERNUrRITION 


69 


of  fluid  ill  connective-tissue  spaces,  which  euhirge  and  fill.  The 
surrounding  tissue  condenses  into  a  cyst  wall.  ((J)  Independently  as 
a  result  of  chronic  irritation  by  foreign  bodies,  extravasated  blood, 
or  parasites,  as  in  dentigerous  cysts^  (P'ig.  31).  Cysts  may  have  but 
one  cavity  (simple  cysts)  or  have  numerous  intercommunicating 
cavities  known  as  loculi  (compound  or  multilocular  cysts) .  Forming 
within  bony  w^alls,  these  may  be  largely  distended,  and  the  walls 
are  usuallj'^  thin.  There  is  generally  a  crackling  sound  produced  upon 
pressure.  Dentigerous  and  other  cysts  are  usually  lined  by  epithe- 
lium peculiar  to  the  part.  The  explanation  of  Malassez,  that  epithe- 
lial remnants  (of  the  enamel  organs)  develop,  forcing  the  connective- 

FiG.  31 


Cyst  of  the  lower  jaw,  having  its  origin  about  an  undeveloped  tooth.       (Garretson.) 

tissue  elements  outward  as  a  covering  to  them,  is  probably  the  correct 
one.  Meanwhile,  fatty  degeneration  of  developed  epithelium  and 
the  collection  of  fluid  account  for  the  fluid  or  pultaceous  character 
of  the  cyst  contents.  This  proliferation  of  epithelial  remnants  is 
well  proved  by  the  development  of  epithelial  products  in  the  interior 
of  dermoid  cysts.     (See  Fig.  98.) 

Dermoid  cysts  are  cj^stic  tumors  of  widely  varying  sizes  found  in 
various  parts,  such  as  the  ovary,  neck,  base  of  brain,  orbit,  etc. 
They  contain  fatty  and  epithelial  debris,  and  are  lined  with  epithe- 
lium, outside  of  which  is  a  corium  with  its  papillae,  and  outside  of 
this  subcutaneous  adipose  tissue.  The  whole  is  inclosed  in  a  fibrous 
capsule  of   connective  tissue.     The  epithelial  lining  may  contain 


1  Green. 


70 


DISTURBANCES  OF  NUTRITION 


and  develop  the  characteristically  dermoid  structures,  hair,  teeth, 
sebaceous  and  sweat  glands  (Fig.  34). 

Broomell^  states  that  the  hair  is  often  several  feet  long,  usually 
of  a  light  brown  color,  regardless  of  the  color  on  the  outside  of  the 
body,  and  becomes  white  as  age  whitens  the  outside  hair,  and  is 
usually  absent  in  dermoids  in  bald  persons.    Hair  follicles  are  present. 

He  states :  "  Dermoids  of  the  mouth  are  usually  found  in  the  hard 
and  soft  palates,  infrequently  in  the  former,  but  when  found  are 
complicated,  while  the  more  frequently  found  in  the  soft  palate 

Fig.  32 


Longitudinal  section  of  a  tooth  from  an  ovarian  cyst:  a,  b,  d,  tissue  filling  absorp- 
tion cavities;  c,  narrow  band  of  connective  tissue  through  which  the  organ  a  received 
its  nourishment;    d,  absorption  of  enamel.     (Miller.) 

are  simpler.  In  these  situations  they  range  from  the  size  of  a  pea 
to  that  of  a  hen's  egg,  the  larger  being  pendulous.  They  are  also 
found  on  the  floor  of  the  mouth  and  dorsum  of  the  tongue.  Brown 
instances  a  case  in  which  one  lay  under  the  jaw  and  extended  down 
the  side  of  the  neck.- 

"The  teeth  range  in  shape  from  the  simple  cone  to  multicusped 
complex  forms,  the     crowns  of  the  same  being  well  formed.     The 


1  Dental  Cosmos,  1905. 


2  Ibid.,  1908. 


DERMOID  CYSTS 


71 


roots  are  usually  not  fully  calcified  or  developed,  or,  perhaps,  partly 
developed.  A  follicular  wall  is  present.  The  enamel  may  be  smooth 
or  pitted. 

"The  cementum  is  usually  absent  or  but  slightly  developed. 

"Radicular  odontomes  evidenced  by  tumor-like  growths  on  roots 
are  due  to  aberration  of  the  dentinal  germ.  The  pulp  canal  was 
always  present  in  cases  examined.  Fusion  of  teeth  has-  occurred  in 
these  cysts.  In  histology  the  teeth  are  similar  to  ordinary  teeth, 
with  some  slight  aberration  due  to  the  peculiar  condition." 

Fig.  33 


Absorption  tissue,  from  cavity  a  in  Fig.  32. 

According  to  Eccles  and  Hopewell-Smith,^  the  teeth  may  be  found 
imbedded  in  alveoli  in  bone;  that  a  small  jaw  with  normal-sized 
teeth  may  exist. 

Miller^  states  that  the  cystic  contents  include  fatty  acid,  oxalic 
acid,  large  quantities  of  tyrosin  and  leucin,  which  substances  furnish 
the  acid  for  the  decalcification  of  teeth  occasionally  found,  but  that 
no  bacterial  action,  such  as  occurs  in  the  second  stage  of  dental 


'  Proceedings  of  the  Royal  Society  of  Medicine. 
-  Dental  Cosmos,  1905. 


72 


DISTURBANCES  OF  NUTRITION 


caries,  could  be  found.    He  stated  that  in  those  teeth  having  living 
pulps  transparency  might  be  found. 

Tumors. — A  tumor  is  a  new  growth  conforming  to  a  degree  to  the 
normal  histology  of  a  part,  but  having  no  physiological  function 
and  no  typical  limit  of  growth.  They  are  classed  as  benign  or  malig- 
nant, accordingly  as  they  are  strictly  localized  and  comparatively 
harmless,  or  tend  to  sap  vitality  and  to  spread  dangerously,  or  to  be 
transferred  to  other  localities  (metastasis). 


Fig.  34 


Portion  of  a,  wall  of  an  ovarian  dermoid  cyst:   a,  wall  of  the  cyst;   b,  projecting  portion 
made  up  of  fatty  and  cutaneous  tissue;   c,  hairs;   d,  teeth.      (Ziegler.) 


The  growth  of  a  tumor  is  attended  by  a  sapping  of  the  vitality  of 
a  sufferer — the  degree  of  the  debility  produced  being  apparently  in 
direct  ratio  to  the  size  and  the  rapidity  of  the  growth.  Besides  the 
size  and  the  rapidity  of  development  of  individual  tumors,  another 
element  determines  their  malignancy,  their  position,  and,  further- 
more, their  occurrence  in  other  parts  resulting  in  multiple  tumor 
formation.  A  tumor  victim  acquires  a  peculiar  appearance — a  cach- 
exia whose  intensity  and  rapidity  of  advance  are  directly  dependent 
upon  the  degree  of  malignancy,  and  the  effects  produced  upon 
general  nutrition  by  the  toxic  substances  entering  the  circulation. 

Tumors  introduce  no  new  form  of  tissue  element;  they  are  repro- 
ductions of  the  cells  of  the  tissues  of  the  body.  They  may  have  the 
same  cell  formation  as  the  tissue  from  which  they  spring,  and  are 


TUMORS  73 

then  called  homologous  tumors;  or  they  may  have  a  different  histo- 
logical structure  from  the  tissue  in  which  they  are  found,  being  then 
called  heterologous  tumors.  For  example,  a  bony  tumor  growing 
from  bone  would  be  homologous;  a  cartilaginous  tumor  growing 
from  gland  tissue  would  be  heterologous. 

Etiology. — The  causes  of  tumor  formation  are  unknown ;  it  has  been 
believed  that  their  growth  is  due  to  parasites,  especially  the  protozoa; 
this,  however,  has  not  been  proved.  A  certain  proportion  of  tumor 
formations,  7  to  14  per  cent.,^  appear  to  be  caused  by  traumatic 
injury;  as,  for  example,  in  cases  of  mammary  tumor,  a  history  of  a 
blow^  or  fall  may  be  at  times  obtained. 

Long-continued,  sluggish  inflammation  appears  to  be  causative 
of  tumor  formation  in  an  unknown  percentage  of  cases.  A  chronic 
irritation  of  certain  portions  of  the  body,  such  as  the  junction  between 
the  mucous  and  skin  surfaces  of  the  lip,  the  sides  of  the  tongue,  etc., 
is  a  frequent  antecedent  to  their  formation.  Ziegler  gives  a  reason- 
able explanation  of  the  origin  of  certain  epithelial  tumors  in  organs 
which  are  undergoing  atrophy;  for  example,  in  advanced  age  the 
connective  tissue  of  the  body  is  undergoing  atrophy  and  there  is 
relaxation  of  its  strata;  the  epithelium  of  the  surface  (or  of  glands), 
still  possessed  of  its  power  of  reproduction,  proliferates  and  invades 
the  connective  tissue,  producing  cancer. 

Cohnheim  advanced  the  theory  that  embryonic  remnants  or 
"rests"  are  included  in  the  tissues  and  in  time  reassert  their  pro- 
liferative powers. 

Tumor  formation  consists  in  the  reproduction  of  the  cells  of  one 
or  more  tissues,  and  in  the  growth  thus  formed  bloodvessels  are 
developed.  Tumors  do  not  contain  nerves,  though  they  may  develop 
in  nervous  tissue. 

"The  bloodvessels  of  tumors  have  comparatively  fragile  and  poorly 
developed  walls.  In  the  malignant  growths  or  rapidly  developing 
tumors  of  any  sort  the  vessels  are  mere  spaces  between  the  tumor 
cells,  with  little  attempt  at  the  development  of  firm  walls. "^ 

About  the  more  slowly  developing  tumors  a  condensation  of  con- 
nective tissue  occurs  in  many  cases,  forming  a  distinct  limiting  wall 
or  capsule  from  which  the  tumor  may  be  enucleated. 

The  two  great  classes  of  tumors,  those  of  mesoblastic  and  those 
of  epiblastic  and  hypoblastic  origin,  may  be  subdivided  into  orders 
according  to  their  histological  peculiarities. 

1  Ziegler. 

2  Stengel,  A  Text-book  of  Pathology. 


74 


DISTURBANCES  OF  NUTRITION 


Classification  of  Tumors. 


TUMORS    OF   THE   MESOBLASTIC   TISSUES. 


Those  usually  benign : 

Bony  tumor,  or  osteoma. 
Cartilaginous  tumor,  or  chondroma. 
Fibrous  tumor,  or  fibroma. 
Fatty  tumor,  or  lipoma. 
Mucous  tumor,  or  myxoma. 
Tumor  of  lymphatic  vessels,  or  lymphangioma. 
Tumor  of  bloodvessels,  or  hemangioma. 
Tumor  of  nerve  fibers,  or  neuroma. 
Tumor  composed  of  neuroglia,  or  glioma. 
Tumor  composed  of  muscle  fibers,  or  myoma. 
Those  usually  malignant: 

Tumors  of  connective  tissues  with  rapid  cell  proliferation  and 
little  intracellular  substance: 

Spindle-celled  sarcoma. 

Round-celled  sarcoma. 

Giant-celled  sarcoma. 
Sarcomata  ]  Angiosarcoma. 

Sarcomatous  cylindroma. 

Melanosarcoma.     . 

Mixed  sarcomata,  as  fibrosarcoma,  etc. 


TUMORS    OF   THE    EPITHELIAL   AND    ENDOTHELIAL   TISSUES. 

Those  usually  benign: 

Papilla  of  skin  or  mucous  membrane — papillomata. 
Tumors  of  epithelial  glands — adenomata. 
Those  malignant: 

"Epithelial  growths  atypically  reproducing  certain  glandular 
or  other  structures  and  showing  a  manifest  tendency  to 
irregular  extension."^ 

Epithelioma  [  Squamous. 

Consists  of  surface  j  Cylindrical 

epithelium  I       (columnar). 

Glandular  carcinoma 

(histologically  resembles  racemose  gland). 
Colloid  cancer. 
Syncytioma  malignum 

(carcinoma  of  placental  site). 


Carcinomata 


'  Stengel,  A  Text-book  of  Pathology. 


TUMORS  75 

Tumors  are  rarely  composed  of  but  one  type  of  tissue;  several 
types  may  be  present,  the  tumor  receiving  its  name  from  the  tissue 
predominating.  When  the  distinguishing  feature  of  a  tumor  is  two 
predominating  tissues,  the  tumor  is  given  a  compound  name;  as, 
for  example,  when,  in  a  sarcomatous  growth,  numerous  large  multi- 
nucleated cells  characteristic  of  bone-marrow  are  found  it  is  called  a 
myelosarcoma.  When  fibrous  and  sarcomatous  tissue  are  distin- 
guishing features  the  tumor  is  called  a  fibrosarcoma. 

Tumors  are  dangerous  in  several  ways :  The  size  of  the  tumor  may 
cause  pressure  upon  important  structures.  The  rapidity  of  growth 
may  sap  the  vitality  of  the  individual.  If  the  tumor  degenerate  or 
suppurate,  it  may  produce  hemorrhages,  or  the  absorption  of  the 
poisonous  products  may  produce  toxemia  with  anemia,  emaciation 
and  weakness,  and  a  train  of  malnutritional  conditions  due  to 
intoxications  (p.  100).  The  metastasis  of  portions  of  tumors  as 
emboli  reproduces  the  tumor  in  a  new  locality.  In  the  connective 
tissues  the  sarcomata  are  the  malignant  types  and  the  sarcomatous 
element  in  a  mixed  tumor  determines  the  malignancy,  e.  g.,  in  fibro- 
sarcoma. In  the  epithelial  tissues  the  carcinomata  are  the  malignant 
tumors,  and  in  mixed  tumors  determine  the  malignancy. 

Malignant  tumors  are  often  associated  with  disturbance  of  the 
general  health  from  their  inception.  They  tend  to  recur  after  abla- 
tion and  either  invade  the  adjoining  tissues  which  may  cause  grave 
local  disturbance  or  the  morbific  material  they  form  enter  the  cir- 
culation or  lymphatics  and  thus  are  transplanted  to  other  localities 
(metastasis) . 

Since  the  malignancy  of  a  tumor  is  due  primarily  to  the  size  and 
the  rapidity  of  its  growth,  it  is  clear  why  sarcomata  are  more 
malignant  than  fibromata,  and  why  some  forms  of  sarcomata  are 
more  malignant  than  others.    To  illustrate: 

Begin  observation  at  the  different  stages  of  connective-tissue 
development,  when  connective-tissue  cells  have  first  divided,  repro- 
duced; the  tissue  produced  is  at  the  indifferent  stage,  as  seen  in 
section  of  the  embryonic  jaw  (Fig.  35). 

Mesoblastic  cells  at  this  early  period  are  in  an  indifferent  stage; 
some  of  the  cells  shown  in  the  figure  will  form  bloodvessels,  others 
will  become  bone  corpuscles,  others  will  form  fibrous  and  others 
muscular  tissue.  This  structure  has  its  analogue  among  tumors 
in  a  soft,  fleshy,  rapidly  growing  growth,  called  the  round-celled 
sarcoma.  As  cells  expend  their  vital  energy  in  three  ways  (nutritive, 
functional,  and  reproductive  activity)  the  embryonic  cells  of  such 
a  growth  may  expend  their  energy  in  nutrition  (growth),  and  will 
then  grow  out  of  the  indifferent  stage  into  a  more  mature  form  of 


76 


DISTURBANCES  OF  NUTRITION 


Fig 


connective  tissue,  the  ultimate  form  of  one  type  being  a  fiber;  an 
embryonic  round  cell  undergoing  a  series  of  form  changes  from  a  small 
round  cell  to  a  long  fiber  (Fig.  36).  The  growth  may  cease  at  any 
stage  of  this  form  change,  the  tumor  composed  of  such  cell  forms 
receiving  a  corresponding  name.     The  embryonic  connective-tissue 

tumors,  as  stated,  are  called 
sarcomas,  the  form  of  the 
cells  composing  them  giving 
them  a  qualifying  title. 

In  Fig.  36  are  represented 
the  stages  of  development 
of  a  connective-tissue  fiber 
from  a  round  cell.  If 
growth  cease  at  stage  1,  and 
the  cell  energy  thereafter 
expend  itself  in  reproduc- 
tion, a  rapidly,  growing 
tumor  composed  of  small 
round  cells  is  formed — a 
small  round-celled  sarcoma, 
markedly  malignant.  If 
the  cells  expend  a  portion 
of  energy  in  growth  of  cell  size,  a  large-celled  sarcoma  is  formed, 
less  malignant  than  the  former.  If  the  cells  expend  a  portion  of 
their  energy  in  forming  intercellular  substance,  reproduction  and 
malignancy  are  less  active.  So  the  spindle  forms,  3  and  4,  represent 
less  rapid  reproduction  and  lesser  malignancy  than  1  and  2,  although 


Porcine  embryo:  ct,  embryonic  connective  tissue 
of  mesoblast.     2.5  cm.      X  250. 


1  2 

®    ® 


Fig.  36 


the  form  4,  which  should  be  of  less  rapid  reproduction  than  3,  because 
of  more  mature  organization,  is  frequently  more  malignant,  because 
less  intercellular  substance  is  formed,  as  shown  in  Figs.  37  and  38, 
the  energy  represented  in  that  process  being  used  up  in  reproduction. 
The  nearer  the  approach  to  the  mature  form  (6,  Fig.  36)  the  slower 
the  growth  of  the  tumor,  which,  when  composed  of  tissue  of  this 
type,  loses  its  fleshy  (sarcomatous)  appearance  and  becomes  fibrous, 
and  is  hence  called  a  fibroma. 

When  a  sarcoma  begins  its  growth  from  bone,  its  histological 
character  is  frequently  modified  (Fig.  39).    It  contains  large  marrow 


TUMORS 


77 


cells  which  have  undergone  incomplete  reproduction,  forming  giant 
multinucleated  cells;  this  is  a  common  form  of  tumor  emerging 
from  the  sockets  of  teeth.    Some  of  the  cells  of  a  sarcomatous  growth 


Fig.  37 


Small  spindle-celled  sarcoma  (from 
a  tumor  of  the  leg) .      X  200.  ^ 


Fig    38 


Large  spindle-celled  saicoma.  To  the  left 
the  cells  have  been  separated  by  teasing,  so 
that  their  individual  forms  are  apparent;  to 
the  right  they  are  in  their  natural  state  of 
apposition,  such  as  would  be  seen  in  a  thin 
section  of  the  tumor.      (Virchow.) 


may  go  on  to  maturity,  while  others  remain  at  some  stage  of  their 
developmental  career.  Malignancy  wdll  be  modified  according  to 
the  amount  of  mature  tissue  formed. 


Fig.  39 


Fig.  40 


Myeloid  epulis  from  lower  jaw:  a, 
multinucleated  giant  cells;  b,  oval  cells. 
X  265.      (Pepper.) 


Adenoma  of  the  breast:  a,  group  of 
glandular  acini;  b,  fibrous  stroma;  c, 
cells  broken  away  from  their  attach- 
ment.     X  265.     (Pepper.) 


Epithelial  Tumors. — Growths  arising  from  epiblastic  or  hypoblastic 
tissues  may  be  benign  or  malignant.  What  are' called  the  adenomata 
may  be  taken  as  the  type  of  the  benign  epithelioma;  that  is,  compara- 


(' 


78  DISTURBANCES  OF  NUTRITION 

tively  benign.  They  present  all  of  the  characters  of  typical  glandular 
tissue;  numerous  acini  lined  with  epithelial  cells  and  surrounded  by 
connective  tissue  (Fig.  40),  Tumors  of  this  type  may  lose  their 
comparative  benignancy  and  become  of  the  succeeding  epithelial 
type. 

Carcinomata. — These  are  growths  arising  from  preexisting  epithe- 
lial tissue,  which  possess  the  characteristics  of  epithelium  developing 
without  limitations  of  a  basement  membrane.  Beginning  upon  a 
skin,  or  mucous  surface,  or  in  a  gland,  the  reproduced  epithelial 
cells  are  not  sharply  marked  off  from  the  connective  tissue  by  a 
limiting  membrane,  but,  gaining  entrance  to  the  alveoli  of  connective 

tissue,    they    proliferate    there,    find 

^^'^-  ^^  their  way  into  lymphatic  vessels  and 

,.  -     '    ■    ~     ^  ,-^N^^^  lymphatic  glands,  and  reproduce  epi- 

^     -  _  '  -  ^-"^.x       thelial    growths     in    such    places    of 

'       "  J       lodgment,    so    that    a    tumor   having 

r>      its  origin  in  one  part  may  give  rise 

to  tumors  in  other  parts  of  the  body 

I       '  — metastasis  (Fig.  41).    Carcimomata 

',7)]  of  the   mouth  are  frequently   due  to 

V'  chronic  irritation,  as  from  smoking  or 

1 V  ?^ '         pipe-stems,  jagged  teeth.     Bay^  states 

\^    '^~'^\,  ^:  that  it  is  rare  in  European  women  while 

lQ/  ^-  /    r  , ,  ( wji^  common  in  men;  that  women  of  Cey- 

^^^rT '  '' 1:^^  Ion  and  India  excite  it  by  betel-nut 

Section  through  an  aggregation       Ciiewmg. 
of  very  young  cancer  cells,  lodged  L^J^g    ^J^g    COUnCCtive-tisSUe    tumorS, 

like  an  embolus  within  a  capillary  .  .  . 

of  the  Hver.  The  parent  growth  typcs  ot  carcmoma  difter  as  to  rapid- 
was  an  adenocarcinoma  of  the     ]^y  ^f  growth  in  their  original  situation 

stomach.  Preparation  stained  with  i     •  i  i  c  s 

hematoxylin.    X  300.    (Ziegier.)       and    m    the    degree    ot    transference; 

these  factors  determine  their  malig- 
nancy. Tumors  of  the  sarcoma  group  may  also  give  rise  to  growths 
in  other  parts,  the  tumor  cells  being  carried  thence  by  lymph 
vessels   or   bloodvessels. 

After  a  period,  tumors  frequently  suffer  such  interference  with 
their  nutrition  that  degeneration  occurs  in  them. 

After  removal,  some  varieties  of  tumors,  both  those  which  infiltrate 
surrounding  tissues  and  those  which  are  metastatic,  show  a  tendency 
to  recurrence;  that  is,  removal  does  not  eftect  a  cure,  and  the  tumor 
upon  reappearance  assumes  another  and  a  more  malignant  character. 

Epithelial  tumors  never  become  tumors  of  the  connective-tissue 

1  Dental  Cosmos,  June,  1913. 


DEFICIENCY  OF  NUTRITION;  HYPONUTRITION  79 

type;  and,  vice  versa,  connective-tissue  tumors  cannot  become 
epithelial  tumors. 

The  distinction  formed  between  epiblast  and  mesoblast  in  the 
embryo  is  maintained  throughout  life.  Tumors  show  a  great  variety 
of  histological  characteristics,  for  which  works  on  general  pathology 
should  be  consulted. 

While  the  treatment  of  tumors  is  not  a  part  of  this  book,  it  may 
be  said  that,  unless  the  cause  of  a  tumor  can  be  located  and  its 
benign  character  determined,  it  is  wise  to  view  it  as  dangerous. 
They  should  be  usually  removed  surgically  unless  inoperable.  The 
a;-rays,  radium  rays,  or  Finsen  light  rays,  etc.,  are  useful  in  some 
cases  after  operation  or  in  inoperable  cases. 

Cooley,  of  New  York,  has  suggested  a  toxin  for  injection  which 
inhibits  sarcoma  and  at  times  cures.  Its  use  after  operation  is  held 
advisable.^ 

The  writer  has  been  urged  to  introduce  material  upon  tumors 
of  the  jaws.  This  seems  inadvisable,  as  space  does  not  permit.  A 
tumor  is  readily  seen  and  should  be  viewed  with  suspicion.  If  not 
dental  as  described  hereafter,  it  should  be  referred  to  a  surgeon 
for  further  diagnosis. 

DEFICIENCY   OF   NUTRITION;   HYPONUTRITION. 

If  the  quantity  or  quality  of  the  blood  delivered  to  a  part  be 
deficient,  the  nutrition  of  the  cells  of  the  part  is  impaired.  First, 
atony,  a  lessened  activity  of  the  vital  processes  of  the  part,  occurs. 
Cell  chemistry  is  disordered,  and  waste  products  are  either  retained 
in  or  about  the  cells. 

The  function  of  the  cells  is  diminished:  If  secretory,  its  secretion 
is  lessened;  if  muscular,  the  cell  has  a  lessened  contractility;  the 
relations  between  nutrition  and  waste  are  disturbed;  the  part 
becomes  physiologically  wearied  sooner  than  usual. 

Hypoplasia. — If  the  process  cause  interference  with  the  develop- 
ment of  an  organ,  so  that  it  is  much  below  normal  in  size,  or  the 
development  of  a  part  is  arrested,  whether  from  lack  of  nutrition 
or  disturbance  of  developmental  cells,  the  resulting  condition  is 
termed  hypoplasia. 

If  the  parts  fail  entirel,y  of  development,  the  condition  is  called 
agenesia. 

Atrophy. — If  the  process  of  hyponutrition  be  marked,  the  waste 
in  a  previously  normal  part  may  exceed  repair,  and  the  part  affected 

'Clinton,  Dental  Cosmos,  1910,  p.  316. 


80 


DISTURBANCES  OF  NUTRITION 


becomes  diminished  in  size  or  atrophied  (Fig.  42,  B).  Atrophy  may 
be  general  or  local.  In  general  atrophy  there  is  a  general  loss  of 
tissue,  due  to  an  excessive  waste  or  faulty  assimilation  of  food  by 
the  tissues.  There  is  a  loss  of  body  weight,  due  first  to  a  loss  of  the 
fat,  later  to  shrinkage  in  the  tissue  cells.  The  shrinkage  in  size  of 
the  tissue  cells  causes  shrinkage  of  the  entire  organ.  The  cells  and 
fat-  may  recover  their  size  when  the  faulty  waste  or  assimilation  is 
corrected.  During  atrophy  many  cells  are  lost  through  the  process 
of  fatty  degeneration  and  removed  by  the  phagocytes  (leukocytes), 
so  that  atrophy  may,  like  hypertrophy,  be  both  simple  and  numeri- 
cal. An  atrophied  part  is  pale  and  shrunken,  contains  less  fluid, 
and  is  tough  and  fibrous.  At  times  the  fibrous  portion  or  connec- 
tive tissue  may  increase  as  the  cells  diminish  (sclerosis).    ■ 

Causes.' — General  atrophy  is  caused:^  (1)  By  a  deficient  supply 
of  food  material  delivered  to  the  tissue  cells.  This  may  be  due  to  a 
primary  food  deficiency  or  any  interference  with  its  preparation  for 
absorption  or  with  its  proper  absorption  or  circulation.-  (2)  By 
excessive  waste  of  the  tissues  generally,  as  in  fevers,  prolonged 
suppuration,  etc.  (3)  By  impaired  vital  activity  of  the  cells  them- 
selves, as  in  senile  conditions. 

Fig.  42 


Adipose  tissue:    A,  normal;    B,  atrophic,  from  a  case  of  phthisis;    a,  single  fat  cell, 
with  cell  wall,  nucleus,  and  drop  of  fat.      X  300.      (Virchow.) 

Local  atrophy  may  be  caused:  (1)  By  a  lessened  circulation  in 
a  part  due  to  obstruction  of  the  arteries,  veins,  or  capillaries,  as, 
for  example,  by  pressure.  (2)  By  diminished  functional  activit}^  or 
disuse  of  a  part,  as  in  the  case  of  unused  muscles  or  even  bones. 
Certain  organs  are  atrophied  or  resorbed  as  a  part  of  the  cycle  of 
life,  e.  g.,  the  umbilical  cord,  the  roots  of  deciduous  teeth,  the  thymus 
gland,  the  mammary  glands  after  the  menopause.  (3)  The  loss  of 
nervous  connection  of  a  part  with  the  nerve  centres  controlling  it 
(trophoneurosis),    or    through    interference    with    nervous    centres 


Green. 


DEGENERATION 


81 


having  trophic  influence  upon  a  part.  (4)  Excessive  functional 
activity  may  cause  atrophy  by  producing  a  degenerative  condition 
due  to  overstimulation. 

Degeneration. — If  cells  have  reached  the  limit  of  their  life  cycle 
or  have  been  subjected  to  influences  markedly  disturbing  their 
nutrition,  the  proteids  of  which  they  are  composed  are  replaced 
by  new  substances  of  somewhat  obscure  origin,  which  appear 
in  the  parenchymatous  cells  and  connective  tissue,  markedly 
altering  the  histology  and  pro- 
ducing a  pathological  anatomy  ^^*^-  ^^ 
peculiar  to  each  form  of  degen- 
eration. If  the  change  is  due  to 
chemical  changes  within  the  tis- 
sues, it  is  a  true  degeneration. 
If  the  new  substance  enters  the 
cell,  it  is  an  infiltration. 

Fatty  Infiltration.  —  In  this 
condition  the  fat  is  found  in 
globules  in  the  cells,  which 
globules  tend  to  coalesce.  The 
nucleus  may  be  pushed  aside. 
It  is  regarded  as  simply  the 
storing  of  fat  in  healthy  cells, 
though  possibly  an  infiltration 
may  occur  in  a  debilitated  or 
degenerated  cell  (Fig.  44). 

Fatty  Degeneration.  —  Fatty 
degeneration  is  a  condition  in 
which  the  pathological  accumu- 
lation of  fat  is  found  in  the 
substance  of  cells.  The  cell 
appears  granular  and  fat-drop- 
lets appear  within  the  substance  of  the  protoplasm  and  give  a  black 
reaction  with  1  per  cent,  osmic  acid.  These  do  not  tend  to  coalesce, 
as  in  the  case  of  fat  infiltration.  "  The  larger  the  amount  of  cell 
albumin  replaced  by  fat  the  nearer  is  the  whole  cell  to  death" ^  (Figs. 
45  and  46). 

Three  theories  are  held  as  to  the  origin  of  the  fat : 

1.  That  the  proteid  of  the  cell  is  changed  to  fat. 

2.  That  fat  is  a  normal  part  of  cell  proteid  and  simply  becomes 
more  visible  because  set  free  through  the  action  of  poison  (such  as 


ae 


Muscle  fibers  in  simple  atrophy. 
(Schmaus.) 


Green,  Pathology  and  Morbid  Anatomy, 


82 


DISTURBANCES  OF  NUTRITION 


bacterial  ferments  or  phosphorus)  acting  upon  the  combinaton.  of 
fat  proteids  in  the  cell.  The  administration  of  phosphorus  to 
animals  produces  it. 

3.  That  the  fat  is  infiltrated  from  the  blood,  as  in  fatty  infiltra- 
tion, but  into  diseased  cells.  Thus  animals  were  poisoned  with 
phosphorus  and  then  fed  with  fat  foreign  to  the  animals;  the 
foreign  fat  was  found  in  the  degenerated  cells. 


Fig.  44 


Fig.  45 


Liver  cells  in  various  stages  of 
fatty  accumulation.  X  300. 
(Rindfieisch.) 


Fatty  degeneration  of  cells:  .  a,  from  a 
cancer;  b,  from  the  brain  in  chronic  soften- 
ing.     X  200.     (Green.) 


Fig.  46 


Fatty  degeneration  of  the  heart,  from  a  case  of  pernicious  anemia.  The  protoplasm 
is  replaced  by  globules  of  various  sizes  stained  black  by  osmic  acid.  The  outlines  of 
the  fibers  are  irregular,  owing  to  inequality  in  their  distention.      X  400.      (Green.) 


Causes. — Depression  of  vitality  is  always  the  proximate  cause, 
and  as  primary  causes  producing  this  depression  may  be  mentioned: 

Tissue  starvation  from  any  cause,  as  from  an  altered  food  supply. 
The  lack  of  oxygen  in  acute  hemorrhage  (suboxidation).  The  intro- 
duction into  the  blood  of  toxic  substances,  such  as  mineral  poisons, 


CLOUDY  SWELLING 


83 


e.  g.,  arsenic,  mercury,  or  phosphorus;  chemical  compounds,  as 
carbon  monoxid;  leukomains,  as  in  diabetes  and  chronic  anemia; 
toxins,  as  in  fever  of  bacterial  origin  or  from  a  focus  of  infection. 
Locally,  interference  with  the  circulation,  if  not  sufficiently  over- 
whelming to  produce  death,  may  cause  fatty  degeneration  of  cells 
by  interfering  with  the  food  supply,  as  in  venous  hyperemia,  aseptic 
infarcts,  and  simple  inflammation.  The  products  of  infection  can 
produce  fatty  degeneration  in  the  cells  of  the  inflamed  area.  (See 
Pathology  of  Inflammation.) 

Fig.  47 


Cloudy  swelling  of  kidney  epithelium:  a,  normal  epithelium;  b,  epithelium  begin- 
ning to  be  cloudy;  c,  advanced  degeneration;  d,  cast-off  degenerated  epithelial  cells. 
From  a  preparation  which  had  been  treated  with  ammonium  chromate.  X  600. 
(Ziegler.) 


In  areas  which  have  undergone  fatty  degeneration  a  cheesy  sub- 
stance may  be  formed  out  of  the  degenerated  elements  existing 
in  the  part.  The  fluid  is  gradually  absorbed  and  a  mass  composed 
of  atrophied  cells,  fatty  debris,  and  cholesterin  crystals  is  left.  This 
process  is  known  as  caseation.  Encapsulation  of  the  caseous  mass 
by  fibrous  tissue  may  take  place,  or  its  liquefaction  or  its  calcifica- 
tion may  occur.  Fatty  degeneration  may  occur  in  many  tissues,  and 
the  danger  is  proportionate  to  the  importance  of  the  tissue  involved. 

Cloudy  Swelling  (Parenchymatous  or  Granular  Degeneration). — 
Cloudy  swelling  is  a  change  occurring  in  the  parenchyma  (essential 


84  DISTURBANCES  OF  NUTRITION 

cells)  of  a  part  as  the  result  of  the  presence  of  toxic  substances  in 
the  blood,  or  even  as  the  result  of  aseptic  disturbance  of  nutrition, 
such  as  a  severe  burn.  The  same  causes  which  produce  fatty 
degeneration  may  produce  it. 

Pathology. — The  cell  absorbs  fluid,  swells,  its  contents  become 
granular,  and  the  histological  structure  is  lost.  In  the  early  stages 
the  change  is  albuminous;  no  fat  is  demonstrable;  later,  however, 
it  appears,  so  that  the  change  is  regarded  as  a  first  stage  in  the  pro- 
duction of  fatty  degeneration,  by  which  process  many  of  the  cells 
are  lost,  though  the  organ  may  recover  if  the  patient  withstands 
the  original  disease  (Fig.  47). 

Glycogenic  Infiltration. — Normally,  glycogen  is  found  in  some  other 
tissues  than  those  of  the  liver,  notably  in  muscle.  If  it  appear  in 
tissue  not  normally  containing  it,  or  in  excess  in  those  in  which  it 
is  normal,  a  glycogenic  degeneration  or  infiltration  exists.  It  may 
be  produced  by  any  influence  which  alters  the  behavior  of  cells, 
especially  those  having  secreting  activity  toward  the  carbohydrate 
food  element  (glucose),  as  in  diabetes,  and,  while  mostly  within  the 
cells,  may  exist  in  the  intracellular  tissue.  (Stengel.)  It  is  stained 
brown  by  iodin  and  converted  by  ptyalin  or  amylopsin  into  sugar, 
the  color  reaction  then  not  occurring. 

It  does  not  seem  to  be  clearly  shown  as  a  direct  infiltration  of 
glycogen,  but  rather  as  an  appearance  of  glycogen  in  the  cells,  which 
may  readily  be  glucose  changed  to  glycogen  within  the  cells.  It 
has  not  been  satisfactorily  shown  to  be  a  degeneration  from  proteid 
constituents.     (Stengel.) 

Cook^  calls  attention  to  the  fact  that  the  tissues  become  capable 
of  diverted  action,  and  that  the  glycogen  may,  even  experimentally, 
be  so  acted  upon  by  oxidizing  agents  as  to  be  converted  into  acid 
derivatives,  probably  lactic  acid,  paralactic  acid,  and  sarcolactic 
acid,  and  that  these  may  be  broken  up  by  the  zymotic  action  of 
tissue  cells  or  by  certain  bacteria.  The  degenerative  change  in  the 
tissues  renders  them  susceptible  to  bacterial  action,  as  in  case  of 
the  gum  tissue. 

The  mucous  membrane  of  the  gums  has  been  shown  by  the  same 
author  to  be  capable  of  this  degeneration  if  overstimulated  by  chem- 
ical agents  followed  by  the  use  of  a  stiff  brush,  and  he  argues  that 
acid  derivatives  may  be  liberated  either  by  the  tissue  or  by  bacteria 
in  contact  with  them,  and  thus  possibly  account  for  certain  phases 
of  tooth  destruction,  as  erosion.  He  emphasizes  the  fact  that  infil- 
tration of  tissue,  with  abnormal  quantities  of  a  normal  constituent 

1  Dental  Cosmos,  1907. 


DEGENERATION 


85 


of  the  body,  is  more  likely  to  take  plaee  in  the  lyiiii)h()i(l  and  nuicous 
eells  of  the  Ixnly  than  in  any  other  tissue  strueture. 

Hyaline  Degeneration. — In  Aarious  forms  of  arthritis,  in  arterio- 
sclerosis, during  infection,  in  septic  processes,  and  in  other  condi- 
tious  a  retrogressive  process,  characterized  by  the  appearance  of  a 
homogeneous  proteid  substance,  occurs.  It  is  closely  allied  to  amyl- 
oid, mucoid,  and  colloid  degeneration,  and  to  coagulation  necrosis. 
The  new  tissue  is  of  a  glistening,  waxy,  homogeneous  appearance, 
and  stains  with  great  affinity  with  acid  anilin  stains,  as  acid  fuchsin, 
taking  a  brilliant  red  color.  The  cells  of  the  part  may  show  fatty 
degeneration. 

Location. — Seats  of  interest  are  the  endothelium  of  bloodvessels, 
which  is  proliferated,  making  the  wall  thickened,  and  the  lumen  nar- 
rowed  or   obliterated.     (See 

Endarteritis         Obliterans.)  Fi«  48 

Upon  mucous  membranes  it 
causes  opaque  plates  or 
pseudomembranes.  It  oc- 
curs in  interstitial  tissues 
and  also  within  the  cells. 
Its  proximate  etiology  and 
pathology  are  obscure. 

The  hyalin  material  can 
be  reconverted,  absorbed, 
and  removed.  It  does  not 
injure  the  cells  to  an  extreme 

degree.  It  may  be  converted  into  other  albuminoid  degenerations, 
may  undergo  caseation  and  calcareous  infiltration.  (Stengel.)  It 
has  been  found  in  the  epithelium  of  the  mouth  by  Cook,  but 
without  established  significance. 

Mucoid  Degeneration. — In  this  form  of  degeneration  the  proteid 
protoplasm  of  cells  is  transformed  into  mucin,  a  glycoproteid  charac- 
terized by  affinity  for  basic  anilin  stains,  as  methylene  blue.  It 
occurs  in  catarrhal  mucous  membranes,  connective  tissue,  tumors,  etc. 
Mucin  absorbs  water,  but  is  not  soluble  in  it  or  dialyzable.  In  the 
catarrhal  mucous  membranes  the  goblet  cells  show  excess  in  number, 
and  are  swollen  and  distended  with  mucin.  (Stengel.)  The  cell 
becomes  vacuolated  and  the  nucleus  granulates  and  stains  with  a 
basic  stain.  About  tlie  necks  of  teeth  the  mucus  becomes  stringy  and 
tenacious,  its  chemical  and  physical  character  being  changed  and 
chondroitin  present.    (Cook.)^ 


Hyalin  degeneration  of  small  vessels  in  the 
cord.      X  350. 


1  Dental  Cosmos,  1907. 


86 


DISTURBANCES  OF  NUTRITION 


According  to  this  author  this  substance  combining  with  water 
might  give  rise  to  sulphuric  acid  in  contact  with  the  teeth.  C18H27 
NSOi7+H20  =  H2S04+Ci8H27NOi4.  Mucic  acid  might  be  produced 
from  glycuronic  acid  found  in  mucin.  Cook  observed  mucoid  degen- 
eration of  epithehal  cells  and  submucous  structure  in  cases  in  which 
strong  astringents  were  used  on  the  mucous  membrane;  the  con- 
traction of  the  cells  caused  a  retention  of  mucin  leading  to  a  chemical 
change  in  the  mucin  itself.    (See  Erosion.) 

Fig.  49 


Colloid  cancer,  showing  the  large  alveoli,  within  which  is  contained  the   gelatinous 
colloid  material.      X  300.      (Rindfleisch.) 


Colloid  Degeneration. — This  consists  of  the  abnormal  appearance 
of  a  non-dialyzable  substance  like  mucin,  but  differing  from  it  in 
preference  for  acid  stains,  by  not  being  precipitated  by  acetic  acid 
and  alcohol,  by  lack  of  absorption  of  water,  also  by  causing  a  more 
profound  disturbance  of  cells  in  which  this  is  found  and  in  which 
it  remains  much  longer.  Salts,  as  calcium  oxalate,  are  apt  to  be 
precipitated  in  it,  and  may  be  again  dissociated.  The  etiology  is 
obscure,  but  probably  analogous  to  that  of  mucoid  degeneration. 

Dropsical  Infiltration. — This  is  an  infiltration  of  an  excess  of 
plasma  into  cells.  It  is  a  part  of  cloudy  swelling,  or  may  occur  as 
large  droplets  of  plasma  enlarging  the  cell  compressing  the  nucleus 
and  protoplasm,  and  may  even  cause  the  cell  to  burst.  Fatty  degen- 
eration of  the  protoplasm  may  occur  as  a  sequence  to  dropsical 
infiltration.  The  process  occurs  in  general  dropsy,  in  burns,  in  skin 
lesions  connected  with  vesiculation,  and  in  inflammation  of  organs. 

Lardaceous  Degeneration.— This  type  of  degeneration  is  known  as 
amyloid,  albuminous,  or  waxy.  The  formation  of  the  material  from 
which  this  condition  derives  its  name  is  preceded  by  an  unknown 


CALCAREOUS  INFILTRATION 


87 


type  of  degeneration  of  the  cells  of  the  part  afl'ected.  The  degenera- 
tive processes  appear  to  be  the  result  of  long-continued  suppuration 
due  usually  to  tuberculous  disease.  In  the  connective  tissue  about 
the  degenerated  cells  (not  in  the  cells)  a  substance  akin  to  albumin 
is  deposited,  which  causes  swelling  and  a  pseudohypertrophy  of  the 
organ  affected.  The  substance  gives  a  reaction  with  iodin  resem- 
bling that  of  starch;  hence  the  name  amyloid  {amylum,  starch).  It 
may  affect  any  organ  of  the  body.  It  usually  appears  first  in  the 
connective  tissue  lying  between  the  inner  and  middle  coats  of  small 
arteries.  The  swelling  caused  by  the  infiltration  markedly  lessens 
the  caliber  of  the  vessels  and  diminishes  the  nutritive  supply  of  the 
parts  supplied  by  the  artery,  which  may  lead  to  fatty  degeneration 
and  atrophy  of  the  insufficiently  nourished  parts. 

Fig.  50 


Calcareous  infiltration  of  renal  epithelia.     From  the  edge  of  an  old  infarct;    a  few 
tubules  still  to  be  recognized.      X  250.     (Sclimaus  and  Ewing.) 

Calcareous  Infiltration. — In  tissues  which  have  undergone  pre- 
vious degeneration,  calcium,  sodium,  or  magnesium  salts  may  be 
deposited  as  an  infiltration  from  the  blood  plasma.  The  parts  are 
thus  petrified.    The  cells  take  no  active  part  in  the  process.^ 

It  is  believed,  however,  that  the  deposit  of  salts  in  the  dying  tissue 
is  more  than  a  mere  precipitation,  and  that  calcification  results  from 
a  combination  of  the  salts  with  an  albuminous  base  and  with  fatty 


1  Green,  Pathology  and  Morbid  Anatomy. 


88  DISTURBANCES  OF  NUTRITION 

acids,  such  an  affinity  being  favored  by  the  degenerative  changes. 
Ordinarily,  the  carbonate  and  phosphate  of  calcium  are  the  infiltra- 
ting salts,  but  in  gout  uric  acid  salts  are  deposited,  owing  to  an  excess 
of  uric  acid  in  the  form  of  biurates  and  quadurates  in  the  body  fluids. 
A  sluggish  circulation  in  the  part  favors  the  deposition  of  the  salts. 
The  calcification  may  occur  in  both  the  cells  and  in  the  intercellular 
substance.^  (See  Calcific  Degeneration  of  the  Pulp.)  In  the  early 
stages  the  salts  are  found  as  fine  granules  in  the  intercellular  substance. 

"The  white,  fibrous  tissue  is  the  form  of  connective  tissue  usually 
affected,  but  concretions  may  occur  in  the  connective  tissue  sur- 
rounding the  bloodvessels. "- 

As  a  secondary  process  after  degeneration,  calcification  of  the 
middle  coats  of  the  arteries  may  occur,  rendering  them  inelastic. 
This  renders  them  incapable  of  regulating  the  blood  supply  to  parts, 
and  these  suffer  more  or  less  nutritive  disturbance,  and,  in  some  cases, 
actual  death  of  the  part  (gangrene).  Calculi  are  found  in  tumors  at 
times.  Many  forms  of  free  calculi  are  formed  in  the  body.  These 
occur  most  frequently  in  ducts  or  cavities  lined  with  epithelium, 
e.  g.,  the  salivary  ducts  and  the  bladder. 

"All  free  concretions  have  an  organic  basis  or  nucleus,"  with 
which  are  combined  the  calcium  salts,  oxalates,  cholesterin,  etc., 
making  up  the  inorganic  or  crystallizable  part  of  the  combination. 
The  organic  part  may  consist  of  inspissated  feces,  as  in  enteroliths, 
mucus,  or  mucin,  as  in  the  calculi  upon  the  teeth;  epithelial  scales, 
mucus,  etc.,  in  the  urinary  passages.^  The  fine  crystals  or  granules 
are  probably  soluble  in  some  cases.  The  larger  calculi  are  probably 
permanent  and  cause  degeneration  of  adjacent  tissue. 

Calcareous  infiltration  is  clearly  to  be  distinguished  from  the 
normal  calcification  of  the  hard  tissues,  bone,  enamel,  dentin,  and 
cementum.  These  are  composed  of  calcoglobulin,  in  which  calcium 
and  magnesium  salts  are  combined  under  the  superintendence  of 
certain  living  cells  with  albuminous  bases  derived  probably  from 
their  own  substance. 

Pigmentary  Infiltration  (see  Tooth  Development). — Pigmentary 
infiltration  is  the  infiltration  of  coloring  matter  into  the  tissues. 
There  are  four  varieties: 

1.  Extrinsic,  derived  from  outside  the  body,  e.  g.,  coal  dust 
in  lung  tissue  or  general  staining  from  silver  salts  taken  up  in  the 
intestines. 

2.  Hematogenous,  derived  from  hemoglobin  or  its  derivatives. 
The}^  are: 

1  Ziegler,  General  Pathology.  2  j^j^j^  3  D^jf]. 


'      NECROSIS  89 

(a)  Hemoglobin,  dark  red. 

(b)  Hemin,  reddisli  brown  or  bluish  black. 

(c)  Methemoglobin,  brownish  red. 

(d)  Hematin,  dark  brown  or  bluish  black. 

(e)  Hematoidin,  orange  or  reddish  brown. 
(/)  Hemosiderin,  yellowish  or  brownish. 

These  are  decomposition  products  of  hemoglobin.  Hemoglobin 
and  hemosiderin  contain  iron. 

3.  Hepatogenous,  or  biliary. 

4.  Metabolic,  resulting  from  cellular  activity  within  the  body, 
and  termed  melanin. 

The  hematogenous  pigments  are  of  chief  interest,  inasmuch  as 
they  occur  in  the  staining  of  teeth  by  devitalized  pulps  and  sometimes 
by  living  pulps  in  a  state  of  venous  hyperemia.  In  these  discolora- 
tions  there  is  an  analogy  to  the  colors  manifested  in  an  old  bruise, 
which  undergo  various  color  changes  as  the  chemical  character  of 
the  pigment  is  altered.     (See  Moist  Gangrene  of  the  Pulp.) 


NECROSIS. 

Necrosis  (from  nekros,  dead)  signifies,  in  its  broadest  sense,  death 
of  tissue.  It  is  due  to  profound  disturbance  of  its  nutritional  func- 
tion or  to  direct  injury  to  its  elements. 

Necrosis  proper  (per  se)  signifies  death  of  tissue  in  mass  from  any 
cause. 

Necrobiosis  means  the  death  of  cells  through  the  process  of 
atrophy  or  degeneration,  which  are  successive  changes  leading  to 
death. 

Necrosis  of  bone  signifies  the  circumvallation  and  death  of  bone 
through  the  process  of  inflammation,  which  causes  thrombosis  of 
its  vessels  and  cessation  of  its  nutrition.  The  dead  part,  when 
separated,  is  called  a  sequestrum.  The  solution  of  continuity  is 
efl^ected  by  leukocytes  massed  about  the  portion  in  which  nutrition 
has  ceased. 

Caries  of  bone  is  that  form  of  bone  death  in  which  the  bone  is 
honeycombed  and  molecularly  broken  down  rather  than  seques- 
trated.    (See  Osteoporosis.) 

Gangrene  is  a  term  used  to  signify  death,  en  masse,  of  a  part, 
the  soft  parts  being  included.  The  dead  part  undergoes  drying 
(dry  gangrene)  or  putrefactive  softening  (moist  gangrene).  (See 
Gangrene.) 

Etiology. — The  causes  of  necrosis  are  as  follows: 


90  DISTURBANCES  OF  NUTRITION 

1.  Circulatory  obstructions,  as  (a)  stoppage  of  an  artery  siippl}'ing 
a  part,  the  nutritive  supply  being  cut  off  by  any  cause;  (6)  venous 
hyperemia  of  a  part,  the  vein  being  unable  to  carry  oft'  the  blood 
charged  with  cellular  waste,  which  accumulates  about  the  cells, 
intoxicates  them,  and  prevents  access  of  fresh  blood  (food  supply); 
(c)  occlusion  of  the  capillaries  by  any  cause  has  a  similar  effect. 
Inflammation  may  be  placed  in  this  general    class  of  causes. 

2.  Trophic  Disturbances. — The  nerves  controlling  the  metabolism 
of  a  part  being  diseased,  the  part  undergoes  degeneration  and  slight 
causes  produce  necrosis,  e.  g.,  necrosis  of  eyeball  when  excision  of 
the  Gasserian  ganglion  has  been  practised. 

3.  Direct  destruction  of  the  vital  activities  of  cells  by  any  physical 
or  mechanical  agents,  or  chemical  substances,  including  among  the 
latter  the  poisonous  substances  produced  through  the  action  of 
bacteria.     (See  Fig.  77.) 

Injuries,  blows,  the  tension  of  exudate,  pressure,  excessive  heat 
or  cold,  the  passage  of  powerful  electric  currents,  and  the  .r-rays 
are  all  influences  which  directly  injure  or  permanently  destroy  vital 
activities  of  cells.  The  application  of  chemical  agents  which  so  act 
upon  cell  substance  as  to  change  its  character  produces  necrosis. 

While  this  is  particularly  true  of  such  substances  as  powerful 
acids  and  alkalies,  or  alkaloids,  which  immediately  destroy  cell 
integrity,  it  is  also  true  of  milder  agents  acting  for  longer  periods. 
Certain  poisons,  particularly  those  of  bacterial  origin,  paralyze  the 
vital  activities  of  cells,  and  necrosis  results. 

The  occurrence  or  non-occurrence  of  or  the  liability  to  necrosis 
will  largely  depend  upon  the  degree  of  vital  energy  of  cells  prior  to 
the  action  of  the  active  causes  of  necrosis.  Parts  debilitated  from 
any  cause  are  more  liable  to  necrosis  than  those  which  have  suffered 
no  debility.  A  part  chronically  ill-nourished,  subjected  to  the  causes 
producing  degenerations,  is  liable  to  suffer  necrotic  changes,  for  the 
several  degenerations  and  atrophy  are  but  successive  stages  leading 
to  necrosis. 

A  necrosed  part  acts  as  an  irritant  to  the  tissues  about  it,  inaugu- 
rating an  inflammatory  reaction  which  marks  off  the  dead  from 
the  living  parts.  The  dead  part  is  sequestered,  and  hence  is  called 
a  sequestrum,  or,  in  case  of  soft  parts,  a  "slough,"  or  sphacelus. 

Necrosis  may  be  of  several  types,  of  which  the  following  are  the 
chief  forms: 

Coagulation  Necrosis. — When  a  dying  tissue  contains  coagulable 
material  and  the  necessary  ferments,  the  parts  undergo  coagulation. 
(See  Coagulation.)  The  cells  and  parts  about  become  solidified,  the 
cells  lose  their  nuclei  and  do  not  stain  as  usual,  and  the  part  appears 


GANGRENE  91 

glazed,  pale,  and  waxy.  It  occurs  in  suppuration,  and  is  due  to  the 
coagulating  ferments  of  pyogenic  cocci.  (See  Bacterial  Ferments; 
also  Fig.  63.) 

The  thrombosis  of  the  vessels  about  an  area  of  infective  inflam- 
mation is  probably  due  to  the  same  ferments. 

Fat  Necrosis. — This  is  a  peculiar  form  of  fat  death  in  which  the  fat 
is  split  into  glycerin  and  fatty  acid  by  lipase  (a  ferment).  The  fatty 
acid  remains  and  combines  with  inorganic  salts. 

Liquefaction  Necrosis. — This  is  the  death  of  tissue  with  liquefaction 
of  the  proteid  material  in  the  area,  which  is  usually  rich  in  exudates. 
The  process  is  probably  due  to  enzymes  capable  of  liquefying  the 
tissue. 

GANGRENE. 

When  death,  en  masse,  of  a  part  occurs  as  the  result  of  an  inter- 
ference with  its  nutritive  supply,  the  process  is  termed  gangrene, 
regardless  of  the  subsequent  results  in  the  dead  tissue. 

Causes. — It  may  occur  as  the  result  of  an  inflammation  produced 
by  a  particular  bacterium,  as  in  noma  or  malignant  edema;  from 
arterial  obstruction,  as  arterial  thrombosis;  or  capillary  obstruction, 
as  in  freezing  or  venous  obstruction,  may  produce  it.  (See  Venous 
Hyperemia  of  the  Pulp.)  Ergot  may  produce  it  through  contraction 
of  the  bloodvessels. 

Dry  Gangrene. — In  parts  which  ordinarily  contain  but  little 
fluid  the  obstruction  of  the  artery  may  be  associated  with  but  little 
obstruction  of  the  veins  and  lymphatics.  Under  such  circumstances 
the  dead  part  is  drained  of  the  little  fluid  it  contains,  and  a  fresh 
access  of  fluid  is  prevented.  Exposure  to  the  air  aids  a  further  loss 
of  moisture  by  evaporation.  The  conditions  are  not  favorable  to 
the  development  of  microorganisms,  and  the  part  changes  from  pale 
appearance  to  a  dark,  shrunken  one.  The  process  of  gradual  drying 
is  also  called  mummification.  (See  Dry  Gangrene  of  the  Pulp.)  It 
is  usually  circumscribed. 

Moist  Gangrene. — Under  opposite  conditions — i.  e.,  a  venous 
obstruction  with  a  fair  arterial  supply — there  is  much  venous 
engorgement  and  extravasation  of  blood  into  the  tissues,  which  are 
stained  red  by  the  hemoglobin  from  disintegrated  red  corpuscles. 
Abundant  eft'usions  also  cause  the  part  to  be  swollen.  Death  of 
tissue  occurs  from  interference  with  nutrition;  when  bacteria  are  the 
direct  cause,  the  part  is  inflamed  and  edematous.  The  moisture 
present  favors  the  development  of  bacteria,  and  they  enter  the  tissue 
through  the  skin.  Putrefaction  with  the  evolution  of  malodorous 
gases,  such  as  hydrogen  sulphid  (H2S),  hydrogen  phosphid  (HP3), 


92  DISTURBANCES  OF  NUTRITION 

and  ammonium  sulphid  (NH4)2S,  causes  the  part  to  have  an  offensive 
odor. 

If  the  gangrene  be  (hie  to  infective  inflammation,  or  the  surrounding 
tissue  be  debiUtated  from  any  cause,  the  area  of  gangrene  may  spread 
— i.  e.,  invade  the  hving  tissue  (spreading  gangrene).  This  is  prob- 
ably due  to  the  presence  of  bacteria,  which  irritate  and  progressively 
destroy  the  surrounding  tissue.  The  poisons  produced,  if  absorbed, 
may  cause  death.  If  the  adjacent  tissue  be  healthy  and  resistant, 
a  line  of  demarcation  is  established,  consisting  of  leukocytes,  which 
dissolve  all  fibers  or  firm  connections  between  the  dead  and  living 
parts.  Suppuration  occurs  at  the  line,  and  the  dead  portion  is 
separated  as  a  sphacelus  or  slough.    Occurring  in  bone,  this  is  called 

Fig.  51 


Senile  gangrene  of  the  great  toe,  from  a  case  of  arterial  thrombosis.  The  toe  is 
shrunken  and  its  epidermis  is  being  exfoliated.  At  the  line  of  demarcation  the  skin 
has  retracted  (a)  and  the  deeper  parts  are  separating  (6).     (Green.) 

a  sequestrum.  An  ulcerated  surface  is  left.  The  latter  form  is  cir- 
cumscribed gangrene.  If  gangrene  be  deep-seated  and  septic,  sup- 
puration occurs,  which  establishes  one  or  more  fistulse  upon  the 
surface  of  the  body  or  in  one  of  its  cavities.  (See  Moist  Gangrene 
of  the  Pulp.)  A  sequestrum  may  be  cast  out  through  one  of  these. 
Occasionally  the  part  being  internal  is  encysted  and  the  contents 
may  be  absorbed  and  the  sac  calcified.^  In  the  aged  atheromatous 
or  calcareous  changes  in  the  arteries  produce  a  slow  circulation  in 
the  extremities.  A  slight  injury  to  a  vessel  wall  may  induce  extensive 
thrombosis  (which  see).  The  result  is  gangrene  of  a  part  or  all  of 
an  extremity,  known  as  senile  gangrene  (Fig.  51). 

1  Stengel,  A  Text-book  of  Pathology. 


GENERAL  MALNUTRITION  93 


GENERAL   MALNUTRITION. 


By  the  term  malnutrition  is  meant  a  more  or  less  general  dis- 
turbance of  the  metabolic  processes  of  the  cells  of  the  body,  which 
may  simply  lower  the  body  resistance  or  health  standard,  or  may  be 
of  such  profound  character  as  to  incapacitate  an  individual  for 
ordinary  functions. 

According  to  Howell,^  some  fourteen  amino-acids  and  four  di- 
amino-basic  bodies  represent  the  construction  of  the  proteids  of  the 
body  which  individually  may  contain  all  or  a  portion  of  the  list. 
These  amino-acids  and  polypeptids,  making  up  the  proteid-making 
food  material  in  the  blood,  are  thought  to  be  derived  by  synthesis 
in  the  intestinal  wall  or  liver  of  the  elements  derived  from  proteid 
food  taken  at  the  mouth  through  gastric  (peptic)  and  pancreatic 
digestion  in  the  alimentary  canal,  which  are  said  to  be  completely 
hydrolized  therein.  When  these  amino-acids  and  polypeptids 
present  at  the  cell  the  cell  enzymes  construct  such  as  they  require 
into  cell  proteid.  Carbohydrate  materials,  fats  and  salts  and  oxygen, 
are  also  utilized  by  the  cells.  In  cell  catabolism  the  specific  chemical 
substances  which  are  the  waste  products  of  the  special  protoplasm 
of  particular  cells,  probably  go  to  other  organs,  as  the  liver,  and 
are  there  changed.  The  ammonia  salts  are  changed  to  urea,  which 
is  the  most  constant  and  bland  of  nitrogen  excretions.  The  mono- 
amino-acids  and  diamino  bases  are  also  changed  to  urea.  Uric  acid 
is  also  in  part  changed  into  urea,  and  even  food  (as  simple  amino- 
acids)  may  be  formed  into  urea  without  entrance  into  tissue 
formation. 

The  purin  bodies  have  a  common  purin  nucleus  or  basis  which 
with  one  atom  of  oxygen  added  forms  hypoxanthin,  two  atoms  of 
oxygen  added  form  xanthin,  three  atoms  form  uric  acid,  which,  as 
stated  above,  may  be  changed  into  urea.  Adenin  and  guanin,  two 
other  purin  bodies,  are  considered  to  be  hydrolized  by  adenase  and 
guanase  or  deaminizing  enzymes  into  hypozanthin  and  zanthin 
respectively;  these  again  are  oxidized  by  another  enzyme  (zanthin 
oxidase)  into  xanthin  and  then  into  uric  acid. 

Some  purin  bodies  come  directly  from  food  (also  urea,  see  above), 
but  also  in  part  are  formed  in  the  body. 

The  catabolism  of  sugar  in  the  body  is  uncertain,  it  being  thought 
that  enzymes  produce  intermediate  products  which  oxidases  change 
to  carbon  dioxid  and  water  and  that  the  internal  secretion  of  the 
pancreas  is    in   some  way  essential.     The  fats  are  supposed  to  be 

•  Toxt-book  of  Ph.vsiology. 


94  DISTURBANCES  OF  NUTRITION 

changed  into  fatty  acids  and  glycerin  under  the  influence  of  Hpase, 
controlled  by  the  liver  through  an  unknown  series  of  changes. 

If  imperfect  digestion,  assimilation,  or  elaboration  of  food  materials 
or  its  circulation,  or  an  imperfect  relation  between  the  amount  of 
oxygen  and  food  material  at  the  cell  exist,  or  if  a  great  excess  of  food 
material  be  assimilated  which  cells  cannot  appropriate,  and  the 
excess  acts  as  material  to  be  gotten  rid  of,  or  if  the  food  taken  be 
of  an  irritating  nature,  or  if  such  material  as  retained  body  waste 
products,  toxins  derived  from  foci  of  infection,  or  from  alimentary 
canal,  or  drugs  absorbed  are  presented  to  the  cells  in  excess,  or  if 
the  drain  upon  the  body  cells  reduce  the  amount  of  cell  protoplasm, 
and  the  replacement  of  the  cell  constituents  is  not  rapid  enough 
to  restore  the  protoplasm  wasted  in  energy,  it  is  plain  that  a  general 
disturbance  of  body  cells  may  result,  and  the  altered  metabolism 
in  turn  furnishes  its  share  of  irritating,  unfinished  catabolic  products 
to  further  increase  the  general  disturbance  through  the  production 
of  a  pathological  condition  of  the  blood  (a  humoral  condition, 
Michaels).  The  gradual  action  of  one  or  other  of  these  classes  of 
causes,  acting  either  by  starving  the  cells  or  by  irritating  them 
(auto-intoxication),  produces  a  condition  with  tendency  to  diseases 
of  certain  type,  and  the  tendency  is  called  diathesis  (acquired) . 

According  to  Michaels,^  following  Gautrelet,  the  abnormal  vital 
processes  tend  in  mankind  to  pathological  conditions,  which  we 
may  classify  under  two  humoral  conditions  (or  diatheses),  viz., 
hypoacidity  and  hyperacidity.  The  first  state  ("lymphatism")  is 
the  expression  of  a  vital  overactivity,  and  has,  as  consequences,  the 
contagious  diatheses  (scrofula,  tuberculosis,  syphilis) .  The  oxidations 
are  overactive,  and  the  hydrations  are  superior  to  the  normal;  hence 
there  is  a  decrease  in  organic  acidity  and  an  increase  of  saline 
chlorides  excreted  by  the  economy.  Hypoacidity  favors  chemical 
changes  in  the  tissues.  (Ducleaux.)  In  the  hypoacid  diathesis  all 
the  oxidations  are  exaggerated,  and  are  above  the  normal. 

"In  the  hyperacid  diathesis  (arthritism),  gout,  rheumatism, 
sclerosis,  oxidation  is  insufficient;  there  is  incomplete  oxidation 
with  a  consequent  increase  of  organic  acidity  or  hyperacidity,  and 
a  peculiar  state  of  the  organism  characterized  in  a  general  way  by 
a  slowness  in  the  biochemical  changes.  The  reaction  of  the  blood 
with  the  ordinary  reagents  (litmus,  for  example)  is  normally  alka- 
line,^ but  if  we  study  the  distribution  of  the  acids  and  bases  of  the 
blood  plasma  we  see  that  the  reaction  is  really  acid  (Gautrelet, 
Drouin,  and  Hugeounenq),  and  thus  acidity  is  increased  and  the  blood 

1  Sialosemeiology,  Proceedings  Third  International  Dental  Congress,  1900. 

2  Neutral  to  Phenolphthalein  (Howell). 


GENERAL  MALNUTRITION  95 

may  become  relatively  acid  by  the  accumulation  of  acid  waste 
products  which  are  not  eliminated,  the  secretions  and  excretions 
becoming  then  of  acid  reaction.  It  is  on  this  account  that  a  certain 
number  of  chronic  diseases  have  constant  characteristics  in  regard 
to  semeiology;  increase  of  the  normal  acidity  of  the  urine,  as  well 
as  the  increase  in  the  normal  acidity  of  the  saliva."  Following 
Gautrelet,  he  gives  four  effects  of  the  exaggerated  and  retrograde 
processes  that  diathesis  produces:  (1)  a  chemical  modification  of 
the  plasma;  (2)  modifications  affecting  the  chemistry  of  secretions 
and  excretions  (as  detailed  above);  (3)  histological  modifications  in 
the  tissues;  (4)  modifications  due  to  the  creation  of  a  special  field 
for  microorganisms.  It  will  be  seen  that  the  above  effect  begins 
with  a  change  in  the  blood  or  its  contents,  which  successively  acts 
upon  glandular  and  other  cell  physiology  and  later  alters  their 
histology,  and  in  total  may  bring  about  a  predisposition  to  bacterial 
invasion  through  the  loss  of  vital  potential  or  resistance.  The 
hyperacid  diathesis  may  be  inherited  or  acquired  by  individuals 
who  take  a  liberal  supply  of  food  requiring  oxidation  and  take 
insufficient  exercise  in  the  open  air,  while  in  the  hypoacid  the 
oxidation  is  superior  to  normal. 

These  diatheses  are  the  forerunners  of  many  of  the  diseases  of 
malnutrition,  and  evidence  of  approaching  disease  may  be  obtained 
from  both  saliva  and  urine  by  analysis  of  their  contents  through 
physical,  chemical,  and  micropolariscopic  examination  of  either  or 
both  fluids.  The  contents  of  each  fluid  being  taken  out  of  the 
blood  through  glandular  activity  represent  fairly  the  faulty  elements. 
The  presence  of  altered  physical  characteristics  when  fresh  or  upon 
standing,  of  unusual  chemical  substances  determinable  either  by  the 
aid  of  reagents  or  microscopic  or  micropolariscopic  examination, 
leads  to  the  inference  that  unusual  chemical  changes  have  oc- 
curred in  the  cells,  or  that  the  waste  products  found  represent 
an  undue  waste  of  tissue,  or  that  cell  waste  has  been  altered  after 
leaving  cells  or  not  sufficiently  changed  into  the  normal  waste 
products. 

In  the  accentuated  disease  condition  one  or  more  organs,  as  the 
liver  and  kidney,  may  be  diseased,  and  it  may  be  a  nice  point  to 
determine  whether  the  disease  begins  with  the  liver  and  proceeds 
to  the  diathesis,  or  with  the  diathetic  condition  or  its  cause  and 
proceeds  to  disturb  the  liver.  At  the  same  time  the  same  course 
might  act  upon  both;  for  example,  overfeeding  with  food  requiring 
oxidation,  and  this  not  supplied  by  exercise,  could  induce  a  disturb- 
ance of  the  function  of  liver  cells  quite  as  readily  as  of  any  other 
body  cells. 


96  DISTURBANCES  OF  NUTRITION 

According  to  Kirk/  the  disproportion  between  pabulum  and  oxygen 
resulting  in  hyperacidosis  produces  a  greater  ratio  of  carbon  dioxid 
to  oxygen  in  the  blood  than  is  normal.  Temporarily  this  would  be 
corrected  by  the  action  of  the  renal  epithelium  in  which  a  reaction 
occurs  between  the  carbonic  acid  of  the  blood  and  the  basic  phos- 
phates, as  follows:  HNa2Po4+H2Co3  =  H2NaPo4+HNaCo3.  The 
sodium  bicarbonate  formed  i-s  returned  to  the  blood,  maintaining  its 
alkalinity,  and  the  acid  sodium  phosphate  is  eliminated  as  the  normal 
acid  salt  of  the  urine.  In  the  same  way  acid  calcium  phosphate  is 
formed. 

When  the  disproportion  between  pabulum  and  oxygen  are  con- 
tinued, the  suboxidation  becomes  chronic,  the  kidney  is  no  longer 
sufficient  to  maintain  alkalescence  of  the  blood  by  eliminating 
the  excess  of  acidity  as  acid  phosphate,  the  carbonic  acid  seeks 
other  channels  of  elimination,  and  the  epithelium  of  the  buccal 
glands  and  sweat  glands  may  take  up  the  action  normal  to  the 
kidney  and  excrete  acid  sodium  phosphate  and  acid  calcium  phos- 
phate, producing  in  the  case  of  the  buccal  glands  a  certain  class  of 
erosion  of  the  teeth,  and  in  the  case  of  the  sweat  glands  frequently 
giving  rise  to  eczematous  eruptions.  Dental  caries  is  not  ordinarily 
introduced  in  this  stage,  but  if  begun  the  carious  matter  is  changed 
to  a  dark  brown  color,  crumbly,  semihard  texture,  and  the  further 
process  is  one  of  decalcification  rather  than  a  true  carious  process. 

"The  continued  suboxidation  and  hyperacidosis  by  carbonic 
acid  thus  leads  to  the  great  loss  of  basic  phosphates  as  acid  phos- 
phates, which  are  more  readily  soluble  and  osmosed  through  kidney 
epithelium  than  basic  phosphates,  and  for  that  reason  are  rapidly 
eliminated,  thus  establishing  a  phosphaturia,  with  consequent 
phosphatic  starvation  and  ill  health,  as  shown  by  neurasthenia, 
with  its  irritability,  despondency,  migraine,  cerebral  hyperemia,  or 
hysterical  phenomena.  A  point  of  depletion  is  reached  and  they 
are  found  only  in  minute  quantity  in  the  urine  and  saliva.  At  about 
this  time  lactates  of  sodium,  calcium,  and  magnesium,  in  the  order 
named,  appear  in  the  saliva,  then  double  lactates  of  sodium  and 
calcium,  then  lactophosphates  of  calcium  and  magnesium,  then 
oxalate  of  sodium  or  double  oxalate  of  sodium  and  calcium,  while 
oxalate  of  magnesium  may  appear  in  the  urine.  With  the  appearance 
of  the  lactophosphate  a  general  rather  than  a  localized  erosion 
appears.  (See  Erosion.)  The  nervous  irritability  is  markedly 
increased,  and  a  rapid  loss  of  weight  occurs.  Later,  acetone  and 
diacetic  acid  appear  in  the  secretion  along  with  creatin,  and  in  some 

1  Dental  Review,  1903. 


GENERAL  MALNUTRITION  97 

cases  cystin,  at  which  period  profound  mental  torpor,  at  times 
almost  amounting  to  coma,  is  not  infrequently  manifested,  or  there 
may  be  extreme  nervous  irritability  amounting  almost  to  hysterical 
mania. 

"Coincident  with  the  loss  of  the  phosphates,  nitrogen  with  carbon 
as  a  cyanogen  radial  (ammonium  cyanate),  which  probably  should 
have  gone  to  form  urea,  is  lost.  Evidences  of  imperfect  oxidation 
of  proteids  are  manifested  in  the  saliva  and  urine  by  the  presence  of 
lactate  of  ammonia  (a  forerunner  of  urea),  lactate  of  calcium,  creatin, 
acetone,  and  oxalates,  with  increase  of  urate  of  ammonia  and  amor- 
phous urates.  The  urine  often  contains  indican,  especially  in  cases 
complicated  with  disordered  liver  and  habitual  constipation.  The 
saliva  is  usually  constantly  acid,  due  to  the  presence  of  acid  phos- 
phates, and  the  dental  lesions  are  ordinarily  erosion,  or,  where  the 
acidity  is  absent,  pyorrheal  invasion  of  the  peridental  membranes. 
Many  of  these  cases  develop  epithelioma  or  leukoplakia  buccalis, 
or  both  together,  and  in  view  of  the  fact  that  there  is  constant  irri- 
tation of  epithelium  by  the  exudates,  they  may  have  an  etiological 
relation."    (Free  quotation,  Editor.) 

The  diet  indicated  by  Kirk  for  these  cases  would  apply  to  those 
diseases  and  cases  of  pyorrhea  in  which  the  predisposition  is  due  to 
this  diathetic  fault,  and  consists  in  reducing  the  necessity  for  oxygen 
by  largely  eliminating  the  carbohydrate  portion  of  the  diet.  Suc- 
culent vegetables,  gluten  bread,  milk,  albumin,  and  a  moderate 
ration  of  proteids  in  the  shape  of  fish,  oysters,  game,  light  meat  of 
fowls,  are  allowed.  Small  doses  of  phosphorus,  or  of  arsenic  iodid, 
and  glycerophosphates  of  lime  and  soda  are  continuously  adminis- 
tered. The  exercise  and  rest  are  adjusted,  and  attention  is  given  to 
general  hygiene. 

"Michaels  found  the  saliva  of  but  few  individuals  to  be  in  a 
perfectly  normal  condition  and  the  teeth  perfect,  while  most  of 
them  are  out  of  equilibrium  and  the  teeth  are  affected  either  by 
caries  or  erosion  or  pyorrhea  alveolaris.  He  states  that  lesions  of  the 
liver  and  kidneys  cause  the  appearance  of  acid  waste,  also  that  the 
organism  constantly  produces  acids,  such  as  uric,  oxalic,  lactic, 
volatile  fatty  acid,  etc.,  which,  under  normal  conditions,  are  also 
destroyed,  but  that  abnormal  conditions  arise  which  retard  the 
oxidations  of  these  organic  acids,  which  must  then  accumulate  in 
the  organism  among  the  waste  products  arising  from  incomplete 
dissimilation;  many  have  acid  properties. 

"The  serum  of  venous  blood,  while  weakly  alkaline,  has  a  real 
acidity  (acid  elements)  stronger  than  that  of  arterial  blood.  Fever 
is  accompanied  by  an  acidity  of  the  blood,  as  in  diabetes  (/3-oxy- 
7 


98  DISTURBANCES  OF  NUTRITION 

butyric  acid),  rheumatism,  arthritism  (gout).     The  alkaUnity  is  re- 
duced (real  acidity  increased)  in  anemia,  leukemia,  and  all  cachexias. 

"He  regards  the  liver  as  determining  the  majority  of  nutritive 
changes,  and  that  it  suffers  from  the  influence  of  all  sorts  of  toxins, 
whether  the  result  of  microbic  activity  or  due  to  an  excess  of  alkaloids 
(leukomains) .  The  cells  of  diathetic  individuals  constantly  elabo- 
rate products,  some  of  which  are  positively  poisonous  to  the  hepatic 
gland.  The  acid  salts  and  biliary  pigments  are  toxic.  Their  absorp- 
tion is  deleterious  and  the  inactivity  of  the  hepatic  cells  creates  a 
danger  to  the  organism.  The  danger  arises  from  the  fact  that  the 
liver  has  to  eliminate  from  the  circulation  all  kinds  of  debris.  If 
the  neutralization  of  the  products  of  fermentation  is  incomplete; 
if  the  harmful  ammoniacal  compounds  have  not  been  changed 
into  urea;  if  the  liver  does  not  have  a  reserve  of  glycogen,  or  if  its 
generators,  which  are  supposed  to  play  a  role  in  the  metamorphosis 
of  alkaloids,  if  through  its  inactivity  there  is  a  retention  of  waste 
products,  the  secretions  are  necessarily  contaminated  with  the  morbid 
principles;  the  toxic  products  present  in  the  blood  poisons  the 
organism  and  constitutes  the  different  diatheses  (auto-intoxication)." 

This  conception  includes  the  views  of  physiologists  that  the  liver 
is  both  a  secreting,  excreting,  and  food-elaborating  organ.  He  argues 
that  if  the  bacterial  fermentations,  by  their  presence  or  by  the  pres- 
ence of  their  toxins,  are  capable  of  modifying  the  enzymic  secretions, 
they  necessarily  influence  the  action  of  the  physiological  fermenta- 
tions. It  follows  from  this  that  these  toxic  principles  saturate, 
in  a  given  period  of  time,  the  organic  secretions  and  produce  a 
cacochymic  state  (morbid  state  of  the  body  fluids) . 

Michaels  has  found  in  the  saliva  of  hypoacid  individuals  glycogen, 
albumin,  perhaps  inosite,  mucin,  basic  chlorids  with  ammonia  in 
greater  quantites  than  normally,  sulphocyanids  and  biliary  acid 
in  less  proportion  than  normally,  and  concludes  that  it  is  an  ideal 
medium  for  the  development  of  microbic  contagion.  He  has  found 
glycogen  in  the  saliva  of  adolescents  generally,  and  susceptible  of 
reduction  and  fermentation  under  the  influence  of  ptyalin  in  the 
presence  of  earthy  salts,  a  fact  emphasized  by  Kirk  with  a  view  to 
its  establishment  as  a  prominent  factor  in  susceptibility  to  caries 
(which  see).  In  the  saliva  of  hyperacids  he  found  sulphocyanids 
and  mineral  and  organic  acids,  acid  phosphates  of  sodium  and  potas- 
sium, ammoniacal  oxalates,  biliary  elements,  and  urobilin  in  greater 
proportions  than  normally. 

The  increased  importance  of  the  consideration  of  metabolic 
diseases  in  their  relation  to  dental  diseases  by  the  dentist  warrants 
the  introduction  of  a  brief  summary. 


GENERAL  MALNUTRITION  99 

Inanition. — This  is  ultimately  tissue  starvation,  whether  due  to 
any  of  the  following  causes: 

1.  Want  of  proper  amount  of  food. 

2.  Gastric  diseases  interfering  with  digestion  by  altering  the 
quality  or  quantity  of  hydrochloric  acid  or  pepsin. 

3.  Disease  of  the  liver,  etc. 

4.  Abnormal  intestinal  digestion. 

5.  Occlusion  of  the  sorbefacients  by  retained  excrementitious 
matter  or  other  local  disease. 

Effects. — The  tissues  are  not  properly  supplied  with  food  to 
maintain  themselves,  and  waste  exceeds  repair;  the  unimportant 
parts  are  first  consumed  and  make  good  the  deficiency.  The  surplus 
food  materials,  first  the  fats,  are  first  consumed,  then  the  carbo- 
hydrates, next  the  nitrogenous  tissues,  first  muscles  and  glandular 
organs,  and,  lastly,  the  osseous  and  nervous  tissues. 

This  is  general  atrophy  necessarily  accompanied  by  degeneration. 
There  is  loss  of  energy  and  temperature,  and  the  vital  organs  are 
weak;  death  occurs  from  exhaustion. 

Overfeeding. — The  excessive  use  of  proteids  in  food  leads  to  a 
necessity  for  elimination  from  the  blood  of  the  excess  absorbed,  and 
to  intestinal  fermentation  of  the  unabsorbed  excess.  The  proteid 
food  maintains  the  proteid  equilibrium,  and  any  more  than  is 
required  for  this  is  in  excess. 

Energy  is  largely  supplied  by  the  carbohydrates  (eventually 
glucose)  and  the  fats.  An  excess  of  these  leads  to  the  storing  of  fat 
to  a  degree  normal  and  useful  as  a  reserve,  but  in  combination  with 
a  sedentary  mode  of  life,  pathological  fat  or  obesity,  in  which 
oxidation  is  reduced.  A  tendency  to  fat  production  exists  in  in- 
dividuals. The  presence  of  food  excess  means  an  overstimulation 
of  metabolism  with  possible  alteration,  which  may  lead  to  general 
disease  of  malnutritional  type  and  predispose  to  infections,  etc. 

Excessive  Tissue  Destruction. — The  tissues  may  be  excessively 
wasted  by  many  causes,  and  in  many  cases  the  food  supply  is  defi- 
cient as  well.    These  causes  are,  briefly: 

1.  Fevers. 

2.  Continuous  hemorrhage. 

3.  Long-continued  suppuration. 

4.  Tumors,  especially  carcinoma. 

5.  Chronic  infectious  diseases,  as  tuberculosis. 

The  increased  waste  is  due  either  to  increased  oxidation  of  the 
proteid  elements,  due  to  stimulation  of  nervous  centres  controlling 
catabolism,  or  to  the  ferment  contained  in  the  toxic  substances 
produced  and  entering  the  blood,  which  may  cause  cellular  waste 


100  DISTURBANCES  OF  NUTRITION 

in  the  effort  to  produce  antitoxins  (see  Ehrlich's  Side-chain  Theory), 
while  at  the  same  time  normal  food  appropriation  is  interfered  with 
if  the  amount  of  food  supplied  is  not  indeed  lessened,  as  in  continuous 
hemorrhages. 

Intoxications. — These  may  be  divided  into  extrinsic  and  intrinsic; 
intoxications.    The  principal  classes  are: 

1.  Intestinal  Intoxications. — In  intestinal  putrefaction,  particularly 
in  constipation,  the  aromatic  products,  acetone,  tyrosin,  indol, 
skatol,  phenol,  cresol,  and  paracresol,  may  be  absorbed  and  produce 
a  form  of  intoxication  of  tissue  cells  which  lowers  the  vital  potential 
of  all  cells  and  the  resistive  force  of  tissues  to  bacterial  infection. 
In  intestinal  putrefaction  in  children  a  marked  readiness  of  the 
muscular  system  to  fatigue  has  been  noted,  also  in  cases  of  persons 
who  have  suffered  from  indicanuria  for  a  long  time,  showing  a  mark- 
edly poisonous  effect  upon  muscle  and  probably  upon  other  tissue. 

The  absorption  of  indol  and  its  modification  in  the  liver  lead 
to  its  appearance  in  the  urine  as  indican,  or  indoxylsulphate  of 
potassium,^  which,  therefore,  indicates  an  abnormal  intestinal  putre- 
faction with  absorption  of  deleterious  products.^ 

That  indican  in  the  urine  is  caused  by  abnormal  tissue  metab- 
olism is  not  well  supported  by  evidence.^ 

It  is  found  in  carcinoma  and  chronic  peritonitis.  It  is  generally 
present  when  suppurations  are  in  progress;  probabl}'^  indol  is  ab- 
sorbed from  the  focus  of  putrefaction.  The  ingestion  of  pus  from 
pyorrheal  pockets  in  the  mouth  may  easily  lead  and  has  led  to-  chronic 
gastritis  and  intestinal  putrefaction,  in  which  latter  Bacillus  coli 
communis  plays  an  important,  assistant  part.  The  liver  may  be 
disordered  primarily,  thus  favoring  the  condition  owing  to  lessened 
formation  of  bile,  or,  secondarily,  owing  to  its  increased  function 
as  a  poison  destroyer.  The  intestinal  putrefaction  causes  the  forma- 
tion of  indol,  etc.,  thus  leading  to  the  presence  of  indican  in  the 
urine.  The  excessive  use  of  proteid  food  not  only  overloads  the 
intestine,  but  invites  putrefaction  therein;  also,  the  amount  absorbed 
being  excessive,  the  eliminative  functions  are  overtaxed,  leading  to 
disease. 

2.  Drug  Intoxication. — The  use  of  arsenic,  phosphorus,  or  other 
inorganic  poisons,  or  the  vegetable  alkaloids,  as  morphin,  cocain, 
atropin,  etc.,  or  the  continued  contact  with  lead  salts,  all  un- 
doubtedly   affect   metabolism — some    beneficially — when    employed 

1  Thompson's  Practical  Medicine. 

-  Test  for  indican:    Add   nitric   acid   to   urine — shake   with   chloroform — a  bluish 
color  is  imparted  to  the  chloroform  on  standing. 
'  Leathes,  Problems  in  Animal  Metabolism. 


GENERAL  MALNUTRITION  101 

ill  suitable  doses  in  diseased  conditions,  or  injuriously  in  continued 
excessive  use.  Thus  atropin  in  small  doses  checks  secretion — e.  g.,  of 
the  salivary  and  mammary  glands.  Phosphorus  continued  produces 
fatty  degeneration. 

3.  Bacterial  Intoxication. — The  toxic  products  of  l)acterial  action 
(apart  from  the  aromatic  products),  as  the  ptomains  and  albumoses 
(toxins),  act  as  ferments  upon  proteid  tissue,  causing  cellular  waste 
either  by  ferment  action  (destruction)  or  by  stimulation  of  the  cells, 
either  directly  or  through  the  nervous  system,  leads  to  the  produc- 
tion of  antitoxic  substances  in  excess,  which  by  Ehrlich  are  claimed 
to  be  discharged  into  the  blood.  No  doubt  the  cell  is  also  rendered 
less  capable  of  anabolism.  (See  Side-chain  Theory.)  This  is  seen 
in  fevers  in  which  emaciation  (excessive  waste)  is  proved  by  the 
increased  output  of  ufea. 

4.  Intrinsic  Intoxication. — In  this  class  may  be  placed  all  intoxica- 
tions produced  by  substances  originating  in  excess  within  the  body 
proper  as  a  result  of  metabolic  disturbance,  resulting  from  disease  of 
the  nervous  centres  controlling  metabolism  or  of  organs  which  fail  to 
perform  their  duty  of  elaboration  for  metabolism  or  elimination  or 
elimination  proper,  in  part  or  entirely.  In  some  cases  compensatory 
elimination  by  other  organs  occurs,  which  may  be  effectual  or  may 
lead  to  disease  of  said  organ  or  organs.  A  good  example  of  com- 
pensatory elimination  is  seen  in  health  during  sudden  changes  of 
atmospheric  temperature.  Thus  on  the  warm  days  perspiration  is 
free  and  elimination  by  the  urine  lessened ;  the  avenue  of  elimination 
is  largely  reversed  on  the  cold  days.  These  intoxications  may  also 
be  classed: 

Uremia. — In  this  there  is  a  retention  of  urea  (as  ammonium 
carbonate  or  its  congeners)  in  the  system  which  should  be  eliminated 
in  the  urine.  The  body  cells  are  chronically  or  acutely  poisoned, 
according  to  the  degree  of  the  retention,  death  resulting  in  the 
complete  form.    Nephritis  is  a  common  cause. 

Diabetes  Mellitus. — In  this  disease  probably  the  essential  lesion 
is  a  hyalin  degeneration  of  the  islands  of  Lai^gerhans,  of  the  pan- 
creas, or  injury  to  the  floor  of  the  fourth  ventricle  of  the  brain 
(diabetic  centre),  which  may  be  caused  by  even  strong  mental 
emotion,  as  grief. 

Carbohydrate  assimilation  is  interfered  with:  an  increased  amount 
of  sugar  appears  in  the  blood  (hyperglycemia)  and  urine  (glyco- 
suria), and  the  cells  are  unable  to  appropriate  it.  Protein  destruction 
with  increased  production  of  urea  occurs   (excessive  waste). ^     An 

1  Stengel,  A  Text-book  of  Pathology. 


102  DISTURBANCES  OF  NUTRITION 

excess  of  phosphoric  and  sulphuric  acids,  jS-oxybutyric  and  diacetic 
acids  are  formed  or  retained,  and  hyperacidosis  results. 

The  sugar  in  diabetes  is  probably  first  formed  from  carbohydrates, 
later  from  proteids,  the  carbohydrate  radicals  being  probably  dis- 
sociated in  the  proteid  disruption. 

Therefore,  patients  who  form  sugar  after  the  elimination  of  sugar 
from  the  diet  furnish  a  grave  prognosis.  The  chief  aim  in  the  treat- 
ment is  the  almost  entire  elimination  of  carbohydrate  food  or  proteid 
food  containing  glycogen.^  All  cells  have  a  lessened  resistance  to 
bacteria,  as  shown  by  an  increased  tendency  to  pneumonia  and 
tuberculosis,^  and  a  similar  predisposition  to  pyorrhea  alveolaris  is 
probable.  The  opsonic  index  is  lowered  in  all  forms  of  glycosuria 
and,  according  to  Stengel,  immunity  to  bacteria  is  lowered  even  in 
experimental  cases. 

Symptoms. — Great  thirst;  frequent  micturition  (polyuria);  in- 
creased amount  of  urine  and  the  excess  of  sugar  in  it;  indicated  by 
high  specific  gravity  and  analysis;  excessive  appetite;  emaciation; 
dyspeptic  symptoms;  hypochondriasis;  insomnia;  skin  diseases,  as 
furunculosis,  are  common.  The  glycosuria  in  diabetes  mellitus 
may  account  for  the  cervical  caries  seen  in  diabetics  by  introducing 
a  factor  in  lactic  acid  fermentation,  viz.,  glycogen  (starch).  (See 
Dental  Caries.) 

Peculiar  Intrinsic  Intoxications. — Without  question,  intense  emotion 
results  in  the  production  of  intrinsic  intoxicants  having  some  influ- 
ence upon  metabolism.  A  most  notable  example  is  the  classic  one  of 
a  mother,  who,  shortly  after  intense  rage  at  an  insult,  nursed  her 
child,  with  fatal  result  to  it.  In  another  case  a  child  was  poisoned  by 
the  milk  of  a  wet-nurse  who  spent  a  night  in  debauchery  (J.  Lewis 
Smith).  The  causes  were  of  slightly  different  classes,  the  modus 
operandi  much  the  same.  Intense  anxiety  also  has  a  disturbing 
influence.  The  nervous  influence  no  doubt  alters  metabolism,  and 
the  products  act  as  poisons  in  a  degree  corresponding  to  their 
amount. 

Acid  Intoxication. — Many  acids  may  be  accumulated  in  the  blood, 
producing  the  condition  known  as  hyperacidosis  or  general  hyper- 
acidity. The  accumulation  is  probably  the  result  of  an  increased 
production  by  metabolism  or  the  incomplete  reduction  to  urea,  etc., 
of  normal,  acid  cell  excreta.  The  condition  probably  arises  as  the 
result  of  gastro-intestinal  disturbances  or  altered  nerve  influence, 
or  the  failure  of  function  in  an  organ,  as  in  diabetes  in  which  acidosis 
exists.     The  acids  are  carbonic,  lactic,  sarcolactic,  sulphuric,  phos- 

1  See  works  on  Practical  Medicine. 

2  Stengel,  A  Text-book  of  Pathology. 


GENERAL  MALNUTRITION  103 

phoric,  uric,  diacetic,  and  j8-()x\'butyric.  The  syini)t()nis  probably 
result  from  the  acidosis  rather  than  from  any  one  acid. 

Suboxidation  always  accompanies  the  condition.  Some  of  the 
acids  combine  with  the  alkaline  elements,  and,  therefore,  reduce 
the  normal  alkalinity,  while  the  acids  left  disturb  metabolism,  thus 
leading  to  further  disturbances. 

Gout. — Gout,  or  podagra,  is  a  recurrent  non-suppurative  arthritis 
associated  with  the  deposits  of  sodium  biurate  in  the  joints,  and 
often  with  constitutional  symptoms.  It  may  be  acute  or  chronic, 
by  some  thought  always  chronic,  with  occasional  acute  manifesta- 
tion. It  is  largely  hereditary  or  the  result  of  inherited  tendency  to 
luxurious  and  indolent  life. 

The  excessive  rise  of  uric  acid  from  proteid  waste  is  held  to  be  the 
cause  of  the  presence  of  biurates  of  sodium,  as  mechanical  irritants 
to  the  joints,  in  which,  owing  to  increased  age  (thirty  or  over)  and 
its  tendency  to  lessened  use  of  joints,  a  sluggish  circulation  with 
increased  acidity  of  the  fluids  of  the  part  favoring  precipitation  is 
established.  The  salts  crystallize  in  the  synovial  tissue  and  excite 
inflammation.  A  slight  excess  of  uric  acid  in  the  blood  is  sufficient 
if  the  local  conditions  are  as  stated.  Ebstein  claimed  that  degenera- 
tion or  necrotic  changes  in  the  tissues  cause  the  precipitation.  The 
sluggish  circulation  leads  in  this  direction.  (See  Venous  Hyperemia 
and  Calcareous  Infiltration.) 

The  conditions  leading  to  a  rise  of  uric  acid  are  many: 

1.  Richly  cooked  foods,  especially  proteid  and  sugar,  with  wines. 

2.  Sedentary  life  combined  with  the  above,  or  overwork  and  under- 
feeding, with  the  use  of  malt  liquors. 

3.  Chronic  lead  poisoning. 

4.  Defective  elimination;  the  output  in  the  urine  is  lessened  just 
before  the  arthritis  and  increased  after  it.    (Haig.) 

Chronic  Gout. — After  an  acute  attack  in  one  joint  others  may  be 
attacked,  and  tophi  (concretions  of  sodium  biurate)  form  in  the  ear 
or  nasal  cartilages,  joints,  sheaths  of  tendons,  etc.  In  some  cases 
crepitation  of  the  joints  may  be  felt  and  heard.  The  joints  may  be 
distorted  and  enlargements  by  the  tophi  occur;  the  skin  over  them 
may  be  smooth  and  shiny,  but  not  inflamed.  The  neighboring  veins 
are  prominent. 

Constitutional  Symptoms.  —  Complications.  —  Weakness,  anemia, 
cachexia,  digestive  disturbances,  dyspepsia,  gastric  and  intestinal, 
with  constipation,  failing  nutrition,  deformity,  inability  to  exercise 
mental  irritations  and  dulness,  granular  atrophic  kidney,  cardiac 
hypertrophy  and  dilatation  with  arteriosclerosis,  chronic  gastritis, 
asthma,  bronchitis,  cerebral  or  other  thrombosis,  sciatica,  eye-skin 


104 


DISTURBANCES  OF  NUTRITION 


lesions,  obesity,  diabetes,  cholelithiasis,  gravel,  and  vesical  calculi. 
(Thompson.) 

Goutiness. — {(louty  Diathesis). — This  is  the  inherited  or  acquired 
condition  underlying  the  acute  and  chronic  forms  of  gout,  or  a 
tendency  to  gouty  symptoms  in  parts  other  than  the  joints,  as  the 

vital    organs,    skin,  and    nervous 
^^*^-  ^2  tissues.     According  to  Ewart,  "  in 

its  functional  aspect  it  is  due  to 
the  abnormal  acidity  of  tissue  juices , 
while  a  delicacy  of  tissues  is  pro- 
duced or  inherited,  causing  in- 
creased irritability  and  lowered  re- 
sistance.^' The  following  diseases 
and  symptoms  may  be  associated 
as  results,  and  in  themselves  show 
the  force  of  Michaels'  claim  for  a 
general  hyperacid  classification  of 
individuals  with  these  symptoms. 
Vascular  System. — Arteriosclero- 
sis, an  increase  of  the  fibrous 
elements  of  the  arterial  walls  and 
indicated  by  their  thickening  and 
the  high  tension. 

This  induces    overwork   of  the 
heart,  resulting  in  cardiac  hyper- 
trophy, and  this  occurring  in  the 
coronary  arteries  produces  failing  nutrition  of  the  heart  and  myo- 
carditis with  appropriate  symptoms. 

Respiratory  System. — Asthma,  emphysema,  and  obstinate  recurrent 
bronchitis;  bronchial  catarrh  in  the  young. 

Genito-urinary  System. — Uric  acid  sediment  with  hyperacidity, 
hematuria,  urethritis,  oxaluria,  albuminuria,  glycosuria  in  some 
cases,  menstrual  disorders,  and  uterine  and  ovarian  disturbances. 

Nervous  and  Muscular  Systems. — Neuralgias,  muscular  soreness, 
lumbago,  sciatica,  bursitis,  sore  heels,  hemicrania,  or  migraine, 
neurasthenia. 

Digestive  System. — Acid  dyspepsia,  acid  eructation.  Tongue  may 
show  glossitis  or  leukoplakia,  gingivitis,  suppurative  tonsillitis 
(infection  added),  bilious  headaches,  chronic  gastritis,  colic. 

Skin. — Harsh,  dry,  tending  to  eczema,  pruritus,  urticaria,  erythema, 
acne,  pityriasis,  furunculosis,  herpes,  exfoliative  dermatitis,  per- 
spiration acid.  Early  gray  hair,  alopecia.  Nails  have  longitudinal 
striae  and  are  brittle. 


Tophi  of  gout.      (Ziegler.) 


GENERAL  MALNUTRITION  105 

Eyes. — Iritis,  glaucoma,  conjunctivitis.  Lesions  of  retinal  vessels, 
retina  and  optic  nerve,  keratitis  and  panophthalmitis. 

These  symptoms  vary  widely  in  different  subjects. 

The  chief  i)oints  of  interest  to  the  dentist,  apart  from  diagnosis 
of  goutiness,  is  the  peculiar  tissue  delicacy,  and  the  general  hyper- 
acidity as  a  cause.  Without  doubt  this  form  of  auto-intoxication 
(acidosis)  in  some  cases  leads  to  thickening  of  small  arteries  in  the 
pericementum,  leading  to  endarteritis  obliterans,  as  shown  by  Talbot, 
and  while  not  the  only  form  of  chronic  gingival  irritation,  is  prob- 
ably one  cause  predisposing  to  gingival  infection  leading  to  the  more 
complicated,  persistent,  and  recurrent  forms  of  pyorrhea  alveolaris. 

It  may  be  regarded  as  established  that  goutiness  may  exist  and 
lead  to  "  declared"  gout,  or  merely  act  as  a  chronic  tissue  irritant. 

Treatment. — The  accepted  medical  therapeutics  of  goutiness, 
which  lies  within  the  special  province  of  the  dentist,  may  well  be 
given  here.^ 

Diet. — Three  moderate  meals  a  day.  Eating  between  meals  to  be 
avoided.  Any  meat,  except  pork,  once  a  day  only;  fresh  fish,  eggs, 
lean  ham  or  bacon,  oysters  or  shell-fish  at  the  other  meals  if  desired; 
oatmeal,  hominy,  cornmeal,  cracked  wheat,  stale  bread  and  crackers, 
fresh  green  vegetables  and  potatoes,  leguminous  vegetables,  apples, 
oranges,  cream  or  other  cheese  as  proteid,  soups,  tea  and  coffee  in 
moderation,  custard  and  gelatin  preparations.  Alkaline  mineral 
waters,  or  plenty  of  plain  water,  before  meals  and  at  bedtime,  or 
the  tablets  of  lithium  citrate  or  bitartrate  may  be  taken  dissolved 
in  water.  To  be  avoided  are  much  meat,  sweet  dishes  and  confec- 
tionery, pastry,  fried  foods,  pickles,  spices,  curry,  cakes,  griddle 
cakes,  alcoholic  and  malt  liquors. 

Hygiene. — Brisk  exercise  in  the  open  air  to  increase  oxidation 
and  elimination  through  the  induction  of  perspiration,  and  Turkish 
baths  if  no  organic  disease  as  of  the  heart  and  kidneys  exists,  and  then 
only  as  advised  according  to  the  advance  of  the  disease.  Daily  cold 
bathing  with  brisk  rubbing;  wearing  of  woollen  clothing.  Sea  bathing 
or  medicated  baths.  The  bowels  should  be  kept  freely  open  with 
cascara  sagrada  or  aloes  if  necessary. 

Special  Therapeutic  Indications. — For  anemic  and  neurasthenic 
cases.  Fowler's  solution,  with  iron  and  cod-liver  oil,  or  blood-making 
preparations. 

For  feeble  digestion: 

I^ — Tincture  nux  vomicae lUx 

Compound  tincture  gentian  or  cinchona     .       .       .       .       .  f3J 

S  — Take  before  meals. 

1  Acknowledgment  in  part  to  Thompson's  Practical  Medicine. 


106  DISTURBANCES  OF  NUTRITION 

For  constipation,  cascara  sagrada,  aloes,  Carlsbad  water,  thialion 
(a  laxative  salt  of  lithium). 
For  gastric  catarrh  with  constipation  and  high  vascular  tension : 

IJ — Sodium  sulphate 3J 

S. — Take  in  a  half-tumblerful  of  hot  water  one  hour  before  meals,  two  or  three 
times  a  day. 

For  persistent  high  vascular  tension: 

Nitroglycerin       . gr.  y^^  every  three  hours. 

Or, 

Sodium  nitrate gr.  iij  three  times  a  day. 

Or, 

Chloral  hydrate gr.  v  three  or  four  times  a  day. 

Lithemia. — This  is  a  condition  occurring  in  individuals  who 
overfeed,  drink  too  little  fluid,  exercise  little,  and  are  under  various 
nervous  strains  or  overwork.  A  neurotic  disposition  and  stimulants 
enhance  the  disturbances  of  nutrition. 

Cold  weather,  adding  to  the  above  a  lessened  perspiration  and 
increase  of  work  by  the  kidneys,  increases  the  difficulty.  Tobacco 
and  alcohol  increase  the  ill  effects. 

There  may  be  no  symptoms  of  gout  in  even  marked  cases.  There 
is  acidosis  with  lithuria  (uric  acid  in  the  urine)  or  oxaluria;  eventually 
renal,  vascular,  and  hepatic  scleroses  develop,  together  with  liability 
to  localized  inflammation  chiefly  in  serous  membranes,  as  the  pleura 
or  synovia. 

The  hypothesis  is  that  uric  acid  or  some  proteid  toxin  irritates 
the  capillaries  to  contraction,  thereby  raising  vascular  tension,  and 
by  this  twofold  toxic  and  mechanical  action  causing  arteriosclerosis, 
which  in  turn  induces  cardiac  hypertrophy,  sclerotic  kidne}^  changes, 
and  vascular  hepatic  cirrhosis.    It  tends  toward  neurasthenia. 

Symptoms. — Nervous  Symptoms. — Vertigo,  tinnitus  aurium,  in- 
somnia, restlessness,  burning  or  pricking  sensation  in  the  palms  or 
soles,  darting  pains  in  the  limbs,  hebetude  of  mind,  hypochondriasis, 
hemicrania,  or  diffuse  basilar  or  frontal  headache,  general  nervous 
irritability. 

Digestive  Symptoms. — Lost  or  capricious  appetite;  coated  red  or 
dry  tongue,  often  fissured ;  aphthous  ulcers,  thirst,  metallic  taste  in 
the  mouth,  pyrosis,  hiccough,  gastric  oppression,  nausea,  gastralgia, 
vomiting,  flatulence;  constipation  or  irregular,  dark-colored,  frothy 
stool;  palpitation  of  the  heart  (an  hour  or  two  after  meals),  hepatic 
tenderness. 


GENERAL  MALNUTRiriON  107 

Urine. — Scanty,  dark,  stronj"!}'  acid,  of  high  specific  gravity,  with 
often  brick-dust  sediment  of  urates.  Perhaps  temporary  albuminuria ; 
perhaps  inflammation  of  urinarA,'  passage. 

Skin. — Eczema,  pruritus,  urticaria  or  lichen. 

Therapeutics. — The  condition  of  life  should  be  reversed  as  to  previous 
eating  and  drinking,  and  exercise  to  avoid  the  overstimulation  by 
proteid  food  waste  and  to  increase  elimination.  Stimulants  are  to 
be  avoided,  sodium  phosphate  given  for  its  action  upon  the  liver  in 
promoting  the  excretion  of  bile,  and  also  for  its  mildly  cathartic 
effect.  It  also  furnishes  an  element  for  regeneration  of  nervous 
tissue,  and  renders  the  body  fluids  more  alkaline.  Lithium  prepara- 
tions are  of  little  value.  Potassium  acetate,  bicarbonate,  and  citrate 
are  useful.  The  bowels  are  to  be  kept  open.  Headaches  may  be 
relieved  by: 

I^ — Phenacetin gr.  xxxvj 

Salol, 

Caffein aa   gr.  xxiv 

M.  and  ft.  capsulse  no.  xii. 

S. — A  capsule  three  or  four  times  a  day. 

For  the  neurasthenic  cases  treat  with  arsenic  and  glycerophos- 
phates. 

The  diet  is  to  be  regulated  as  in  goutiness.  The  use  of  much  fat, 
meats,  or  carbohydrates  is  to  be  avoided,  to  lessen  the  necessity 
for  oxidation  and  for  work  by  the  liver.  The  use  of  a  largely  vege- 
table diet,  to  render  the  body  fluid  more  alkaline.  Plenty  of  water 
between  meals,  to  flood  the  system.  Hygiene,  rest,  and  exercise,  as 
in  goutiness. 

Rheumatism. — Rheumatism  is  an  acute  fever,  probably  of  infective 
origin,  characterized  by  constitutional  toxic  symptoms,  inflammation 
of  the  joints,  muscles,  serous  membranes,  skin,  or  even  tonsils.  It 
may  be  classified  as  acute,  chronic,  or  muscular  rheumatism. 

Etiology  of  Acute  Rheumatism. — It  may  be  transmitted  to  the 
newborn,  or  a  constitutional  tendency  to  it  may  be  inherited.  It  is 
most  common  to  young  adults  (fifteen  to  twenty-five  years),  but  no 
age  is  exempt.    It  is  most  common  in  males. 

Climate,  exposure  to  cold,  injuries  and  overw^ork  of  parts,  occupa- 
tion inviting  exposure  to  hardships,  chronic  alcoholism,  nervous  shock, 
debility,  starvation,  anemia,  and  chorea  are  other  predisposing  causes. 

The  exciting  cause  is  supposed  to  be  largely  due  to  the  Diplo- 
coccus  rheumaticus,  having  its  origin  in  some  focus  of  infection,  as 
the  tonsil  or  gum  margin.  The  streptococcus  or  pneumococcus  may 
be  absorbed  from  some  focus  of  infection  and  produce  metastatic 
joint  inflammation  similar  to  rheumatism  and  be  isolated  from  the 


108 


DISTURBANCES  OF  NUTRITION 


blood  or  joints  of  rheumatic  patients,  but  it  is  also  induced  by  a  diet 
of  meat  or  the  fermentation  produced  by  overuse  of  sugar  and 
starches,  causing  a  rise  of  lactic  or  uric  acid  in  the  blood. 

Clinical  History. — It  presents  the  following  clinical  difference  from 
acute  gout:^ 


Acute  gout. 

Acute  rheumatism. 

Exciting  cause 

Often  errors  in  eating  and  drinking. 

Sometimes  cold  and  damp. 

First  attack   . 

Commonly  in  one  great  toe. 

Commonly  in  large  joints. 

Later  attacks 

Both  toes,  fingers,  knees,  etc. 

Rare  in  toes,  often  shoulder 
or  hip. 

Appearance   of 

joint 

Color  dark  red,  shiny,  and  tense. 

Lighter  red. 

Pain    . 

Worse  at  night  or  early  morning. 

Migratory    from     joint     to 

localized. 

joint. 

Subsidence     . 

■ 
■ 

Leaves   thickening   and   deformity 
with  repeated  attacks. 

Leaves  normal  joints. 

Tophi        .      . 

. 

In  lobes  of  ear,  finger-joints,  etc. 

Never  present. 

Age  and  sex  . 

Common  in  middle-aged  men ;  very 

Common  in  young  persons. 

rare  in  children. 

children,  and  women. 

Effect  of  treatment  . 

Salicylates  have   but   little   effect; 

Salicylates   have'  marked 

colchicum  marked  effect. 

effect;    colchicum   no 

effect. 

Symptoms. — Pain  and  inflammation  of  joint,  which  may  be  pre- 
ceded by  headache,  indigestion,  constipation,  lassitude,  muscular 
aching,  chilliness,  mild  inflammation  of  tonsils,  pharynx,  and  larynx. 
Tongue  coated,  pale,  and  indented  by  the  teeth;  breath  foul.  Fever 
103°  or  104°  F.,  sometimes  hyperpyrexia.  Sweating  during  the 
height  of  convalescence,  with  acid  odor  from  decomposition  of  fatty 
acid,  but  may  be  neutral  or  alkaline  in  parts  of  same  person,  therefore 
not  an  effort  at  elimination  of  acid. 

Saliva. — ^Acid,  excess  of  potassium  sulphocyanid. 

Urine. — Hj^peracid,  urates  increased,  chlorids  diminished,  uric 
acid  abundant,  sometimes  albuminuria. 

Heart. — Pericarditis  and  endocarditis  in  one-fourth  of  all  cases. 

Mind. — Clear  except  in  hyperpyrexia. 

Skin. — Urticaria,  petechise,  ecchymoses,  purpura,  eczema  at  times; 
subcutaneous  nodules  in  youth. 

Complications. — Conjunctivitis  occasionally;  chorea  frequently. 

Prognosis. — Uncertain  as  to  period  before  recovery;  relapses,  or 
recurrence  common. 

Therapeutics. — Sodium  salicylate  and  oil  of  gaultheria,  internally, 
relieve  the  pains  and  inflammation.  Cold  baths  to  reduce  the  tem- 
perature.    Blisters  as  counterirritants;  protection  from  jarring  by 

1  Thompson's  Practical  Medicine. 


GENERAL  MALNUTRITION  109 

cotton  and  fenders;  guaiacol  with  glycerin,  oil  of  wintergreen,  etc., 
as  local  lotions.    The  diet  is  much  the  same  as  in  gout. 

Chronic  Rheumatism. — This  form  has  much  the  same  etiolog}', 
but  is  more  common  after  the  fortieth  year.  It  appears  in  much- 
used  joints,  and  is  most  common  in  females. 

Morbid  Anatomy. — Fibrous  thickening  and  contraction  produce 
moderate  thickening  and  distortion  of  joints;  atrophy  of  muscles 
about  joints  may  occur. 

Symptoms. — Symptoms  are  of  slow  onset;  general  health  good 
unless  inability  to  exercise  produces  alteration.  Pain  absent  except 
when  joint  is  overworked  or  in  damp  weather.  The  fingers  may  be 
deflected  laterally  and  flexed  by  contraction  of  tendons.  Febrile 
attacks,  101°  F.,  occur  from  time  to  time,  but  the  urine  is  normal. 

Prognosis. — Disease  progressive;  no  recovery,  but  temporary  im- 
provement by  treatment  so  that  the  joints  may  remain  quiescent 
for  years.    Never  fatal. 

Systemic  Therapeutics. — Simple  alkalies  or  alkaline  waters,  arsenous 
acid,  20  gr.  t.  i.  d.,  cod-liver  oil  for  debihtated  and  anemic,  Carls- 
bad salts  or  sodium  phosphate  for  constipation. 

Local.— Drenching  with  hot  (105°  to  110°  F.)  and  cold  (70°  F.) 
water  alternately,  followed  by  massage  and  wrapping  the  joint  in 
flannel.  Sweating  in  an  inclosing  box  with  hot  air,  240°  or  250°  F., 
followed  by  Swedish  movements.  The  lotions  used  for  acute  rheu- 
matism are  also  used.    The  diet  is  much  the  same  as  for  goutiness. 

Muscular  Rheumatism. — In  this  form  of  rheumatism  the  dis- 
turbance is  in  the  muscles,  with  little  constitutional  disturbance. 
The  essential  lesion  is  probably  an  inflammation  of  the  muscles, 
though  the  nerves  may  suffer. 

Symptoms. — Local  tenderness  and  pain  increased  by  every  con- 
traction of  the  muscle.  Pain  stationary,  worse  by  night  and  during 
barometric  disturbances;  oxaluria  in  some  cases. 

Scorbutus  (Scurvy). — This  is  a  subacute  or  chronic  disease,  char- 
acterized by  inanition,  anemia,  and  asthenia,  with  purpura  and  a 
tendency  to  swelling  of  the  gums. 

While  of  doubtful  origin,  defective  hygiene  and  the  use  of  improper 
foods,  especially  the  lack  of  fresh  vegetables  and  fruits,  and  the  use 
of  salted  foods,  the  improper  absorption  of  food  owing  to  chronic 
intestinal  maladies,  as  dysentery,  or  to  cachexias,  as  in  malaria, 
cancer,  and  syphilis,  are  the  chief  causes,  though  infection  has  been 
held  to  act  upon  those  debilitated  by  the  above  causes.  In  young 
children  it  is  due  to  the  use  of  proprietary  foods  instead  of  fresh 
food,  and  appears  mostly  from  the  eighth  to  the  twelfth  month, 
rarelv  before  the  sixth  or  after  the  sixteenth  month. 


no  DISTURBANCES  OF  NUTRITION 

The  circulation  is  feeble  and  the  blood  impoverished. 

The  gums  are  red  and  swollen,  protrude  over  and  between  the 
teeth  if  present,  and  bleed;  the  breath  is  offensive,  owing  to  putre- 
faction of  the  blood. 

The  stomach  shows  great  irritability,  and  there  is  thirst  and  craving 
for  acid  foods. 

The  joints  are  swollen  and  painful,  owing  to  the  hemorrhages. 

The  urine  is  high  colored;  the  acidity  and  temperature  lowered. 

Treatment. — As  a  prophylactic  -and  cure,  lime,  lemon,  or  orange 
juice,  together  with  the  use  of  fresh  vagetables  and  fruit  in  adults, 
or  their  juices  in  infants.  Fresh  milk  modified,  white  of  egg,  and 
beef  juice,  or  breast  feeding,  are  to  be  substituted  for  proprietary 
foods  or  table  feeding  in  infants. 

Rachitis  (Rickets). — This  is  a  disease  found  in  infants,  develop- 
ing typical  deformities  in  the  bones,  and  due  to  a  deficiency  of 
lime  salts  in  them,  in  turn  probably  due  to  an  absorption  of  that 
present,  by  hyperemic  tissue  present,  and  a  diminution  in  the  deposi- 
tion of  a  fresh  supply.  There  is  usually,  also,  hypertrophy  of, the 
liver  and  spleen.  The  prolonged  lactation  of  the  child  upon  unfit 
milk,  poor  in  fat,  and  the  overuse  of  proprietary  foods  lacking  the 
proper  food  elements,  as  farinaceous  food  or  exclusively  a  condensed 
milk  diet.  The  teeth  develop  slowly  and  are  apt  to  be  of  faulty 
structure.  The  general  line  of  treatment  is  much  the  same  as  for 
scorbutus. 

Neurasthenia. — This  is  a  condition  of  nervous  exhaustion,  no 
reserve  nerve  matter  being  held  for  even  slight  effort.  It  is  often 
accompanied  by  nervous  excitability,  insomnia  or  disturbed  sleep, 
apprehension,  melancholia,  failure  of  appetite,  and  feeble  digestion. 

Nervous  energy  is  lost  and  irritability  remains.  It  may  be  caused 
by  continued  excitement  or  overwork  of  the  nervous  system,  and 
responds  to  rest,  regulated  diet,  general  tonics,  treatment  by  glycero- 
phosphates of  lime  and  soda  in  the  serious  cases,  while  in  mild  cases 
exercise  in  the  open  air,  baths,  sea  or  mountain  air,  combined  with 
the  tonic  treatment  and  abstinence  from  stimulants,  effect  a  cure.^ 
In  view  of  demonstrations  upon  animals  that  nerve  tissue  is  actually 
used  up  in  nervous  energy,  the  above  treatment  probably  permits 
a  gradual  restoration  of  the  elements  of  nerve  tissue. 

Oxaluria. — The  increase  of  sodium  and  calcium  oxalate  crystals 
in  the  urine  indicates : 

1.  That  food  rich  in  oxalic  acid  (as  tomatoes  or  rhubarb)  has 
been  used  in  increased  quantit}^ 

1  See  Thompson's  Practical  Medicine. 


GENERAL   MALNUTRITION  111 

2.  That  intestinal  fermentation  is  existent  and  forming  it  from 
glucose.    (Baldwin.) 

3.  That  intrinsic  increased  production  of  oxalic  acid  by  oxidation 
of  uric  acid,  in  turn  derived  from  the  purin  bases  of  the  nucleins, 
and  nucleo-albumin  of  the  tissues  is  present. 

It  frequently  accompanies  the  increase  of  uric  acid  in  the  urine, 
and  is  regarded  by  Simon^  as  due  to  impairment  of  normal  oxidation 
processes  in  the  liver.  Thus  it  may  be  found  in  goutiness  and  lithe- 
mia.  It  is  also  associated  with  dyspeptic  and  nervous  symptoms, 
producing  a  condition  known  as  oxalic  acid  diathesis.  It  also 
sometimes  accompanies  diabetes. 

Continued  oxaluria  may  result  in  the  formation  of  calcium  oxalate 
calculi.  It  is  frequently  associated  with  nervous  irritability,  hypo- 
chondriasis, and  neurasthenia.  Oxalates  are  found  in  the  urine  and 
saliva.    (See  p.  96.) 

Phosphaturia. — The  tribasic,  phosphoric  acid,  H3PO4,  is  a  normal 
product  of  metabolism,  and  like  other  acids  combines  with  salts 
before  elimination.  Its  alkaline  combinations  are  sodium  phosphate, 
Na3P04;  calcium  phosphate,  Ca2(P04)2;  and  magnesium  phosphate, 
Mg3(P04)2,  which  may  also  be  found  in  alkaline  urine.  Its  neutral 
combinations  are  di-sodium  hydrogen  phosphate,  Na2HP04;  calcium 
hydrogen  phosphate,  CaHP04;  and  magnesium  hydrogen  phosphate, 
MgHP04,  all  found  in  the  blood  and  in  neutral  urine.  Its  acid 
combinations  are  sodium  di-hydrogen  phosphates,  NaH2P04,  and 
calcium  di-hydrogen  phosphate,  Ca(H2P04)2,  found  in  acid  urine, 
and  to  which  the  normal  acidity  is  partly  and  chiefly  due. 

Ammonium  magnesium  phosphate  (NH4MgP04+6H20)  or  triple 
phosphate  is  also  found.- 

Many  of  the  phosphates  are  derived  from  the  food,  but  some  are 
formed  by  proteid  catabolism;  one-third  of  all  excreted  is  eliminated 
in  the  intestinal  secretion ;  some  are  eliminated  in  the  saliva,  as  shown 
by  the  formation  of  salivary  calculi.  In  diseases  requiring  increased 
phagocytosis,  as  febrile  conditions,  the  elimination  of  phosphates 
falls,  the  phosphates  probably  being  utilized  in  the  formation  of 
leukocytes.     The  excretion  is  increased  in  diabetes  and  tuberculosis. 

A  very  large  increase  in  the  total  amount  of  phosphates  eliminated 
(7  to  9  grams  in  twenty-four  hours)  is  called  phosphatic  diabetes, 
and  has  been  associated  with  four  classes  of  symptoms: 

(a)  Cases  with  marked  polyuria  and  marked  nervous  symptoms. 

(6)  Cases  preceding  or  accompanying  pulmonary  diseases,  espe- 
cially tuberculosis. 

1  Simon,  Clinical  Diagnosis.  -  Kiike's  Physiology. 


112  DISTURBANCES  OF  NUTRITION 

(c)  Cases  in  which  phosphaturia  alternates  with  or  coexists  with 
glycosuria. 

(d)  Cases  in  which  oxaluria,  polyuria,  and  slight  albuminuria  are 
present,  and  in  which  some  relationship  with  gout  exists. 

An  increase  in  the  amount  of  phosphates  in  the  blood  tends  to  the 
production  of  calculi. 

As  nerve  tissue  contains  a  considerable  amount  of  lecithin  or  phos- 
phorized  fat  essential  to  it,  excessive  drain  upon  this  may  result 
in  a  loss  of  this  substance  by  catabolism,  with  loss  of  phosphates 
doubtless  masked  by  the  preponderance  of  phosphates  derived  from 
the  food. 

This  is  borne  out  by  the  beneficial  use  of  glycerophosphates  of 
lime  and  soda,  rest,  and  general  tonic  treatment  in  neurasthenia. 
(See  p.  110.) 

Albuminuria. — The  presence  of  albumin  in  the  urine  may  be 
either  (1)  transitory,  remittent,  or  cyclic  (recurring  with  regularity), 
as  the  result  of  functional  disturbances,  as  anemia,  adolescence,  in 
general  malnutrition,  after  severe  exercise  or  cold  baths;  or' (2)  due 
to  organic  disease  of  the  kidney,  as  acute  and  chronic  nephritis, 
renal  arteriosclerosis,  and  amyloid  degeneration  of  the  kidhey;  or 
(3)  to  fevers,  as  typhoid  and  yellow  fever,  and  is  due  to  the  presence 
of  bacterial  toxin  in  the  blood;  or  (4)  to  circulatory  disturbances,  as 
organic  heart  disease,  or  to  local  circulatory  disturbances,  as  com- 
pression of  renal  veins  by  a  pregnant  uterus;  or  (5)  to  impeded  out- 
flow of  urine;  or  (6)  to  hemic  changes,  increasing  the  diffusion  of 
albumin,  as  in  scurvy,  leukemia,  pernicious  anemia,  jaundice,  and 
diabetes;  or  (7)  to  toxins  in  the  blood  other  than  febrile,  as  turpentine, 
salicylic  acid,  phosphorus,  arsenic,  etc.,  probably  producing  circu- 
latory disturbances  and  irritation  of  glandular  epithelium  of  the 
kidneys;  or  (8)  to  neurotic  disturbances,  as  epilepsy;  or  (9)  to  in- 
gestion of  excessive  amounts  of  cheese,  eggs,  and  other  albuminous 
food;  or  (10)  to  accidental  admixture  after  urine  excretion  by  the 
kidneys^ 

It  is,  therefore,  like  oxaluria  and  phosphaturia,  more  a  symptom 
than  a  disease. 

1  Simon,  Clinical  Diagnosis. 


Ay/ 


Fcff.vm 

a 

6 

c 

d 

e 

/• 

9 

k   '' 

J 

A- 

/ 

m 

n 

■ 

@ 

# 

^ 

m 

# 

BLOOD. 

(Ehrlich  triple  stain.) 

(Prepared  by  Dr.  I.  P.  Lton.) 

Fig.  I.     TYPES   OF   LEUCOCYTES. 

a.  Polymorphonueieap  Neutrophile.  6.  Polymorphonuclear  Eosinophile.  c.  Myelocyte 
(Neutrophilic),  d.  .'Elosinophilie  Myelocyte,  e.  Large  Lymphocyte  (large  Mononuclear). 
/.  Small  Lymphocyte  (snnall  Mononuclear). 

Fig.  IL     NORMAL   BLOOD. 
.Field  contains  one  neutrophile.     Reds  are  normal. 

Fig.  III.    ANEMIA,  POST-OPERATIVE  (secondary). 

The  reds  are  fewer  than  normal,  and  are  deficient  in  hsemoglobin  and  some'what 
irregular  in  form.  One  normoblast  is  seen  in  the  field,  and  two  neutrophiles  and  one 
small  lymphocyte,  showing  a  marked  post-hsemorrhagic  anaemia,  with  leueoeytosis. 

Fig.  IV.     LEUCOCYTOSIS,  INFLAMMATORY. 

The  reds  are  normal.  A  marked  leueoeytosis  is  shown,  with  five  neutrophiles  and 
one  small  lymphocyte.  This  illustration  may  also  serve  the  purpose  of  showing  tha 
leueoeytosis  of  malignant  turner 

Fig.  V.     TRICHINOSIS. 
A  marked  leueoeytosis  is  shown,  consisting  of  an  eosinophilia. 

Fig.  VI.     LYMPHATIC  LEUKEMIA. 

Slight  anaemia.  A  large  relative  and  absolute  increase  of  the  lymphocytes  fchiefly 
the  small  lymphocytes)  is  shown. 

Fig.  VII.     SPLENO-MYELOGENOUS   LEUKEMIA. 

The  reds  show  a  secondary  anaemia.  Two  normoblasts  are  shown.  The  leueoeytosis 
is  massive.  Twenty  leucocytes  are  shown,  consisting  of  nine  neutrophiles,  seven  myelo- 
cytes, two  small  lymphocytes,  one  eosinophile  (polymorphonuclear)  and  one  eosinophilic 
myelocyte.  Note  the  polymorphous  condition  of  the  leucocytes,  i.e.,  their  variations 
from  the  typical  in  size  and  form. 

Fig.  VIII.     VARIETIES    OF    RED    CORPUSCLES. 

a.  Normal  Red  Corpuscle  (normocyte).  6,  c.  Anaemic  Red  Corpuscles,  d-g.  Podkilocytes. 
h.  Microcyte.  i.  Megaloeyte.  j-n.  Nucleated  Red  Corpuseies.  j,k.  Normoblasts.  I.  Micro- 
blast,    m,  71.  Megaloblasts. 


CHAPTER  V. 


DISTURBANCES  OF  THE  VASCULAR  SYSTEM. 


A  SUITABLE  amount  and  quality  of  blood  normally  flows  through 
the  circulatory  apparatus,  and  is  in  close  relation  to  processes  of 
nutrition. 

The  amount  of  blood  in  the  vessels  may  be  increased  (plethora), 
though  not  permanently.  It  may  be  decreased  rapidly  in  quantity, 
as  by  hemorrhage,  or  its  red  corpuscles  may  be  gradually  lessened 
in  number  (acute  or  chronic  anemia) .  The  proportion  of  white  cor- 
puscles to  red  ones  may  be  increased  abnormally  (leukemia).  The 
hemoglobin  of  red  corpuscles  may  be  deficient  (chlorosis).  Locally 
the  amount  of  blood  in  a  part  may  be  increased  (hyperemia  or 
inflammation)  or  diminished  (ischemia). 

Normally  the  blood  contains  floating  in  the  plasma  5,000,000  red 
corpuscles,  or  erythrocytes,  and  from  5000  to  10,000  (1  to  500  red) 
white  corpuscles,  or  leukocytes,  to  each  cubic  millimeter.  (See  Plate, 
Fig.  II.)  A  marked  increase  in  the  number  of  erythrocytes  is  termed 
polycythemia;  a  marked  decrease,  oligocythemia.  The  temporary 
increase  in  number  of  white  corpuscles  is  leukocytosis;  a  persistent 
increase,  leukocythemia  or  leukemia. 

The  blood  corpuscles  may  be  classified  as  follows: 


Erythrocytes       (non-nu- 
cleated red  corpuscles) 


Normal  to 
blood. 


Normocytes  (normal  size) 


See  Plate, 
Fig.  53  Fig.  VIII 

1,2,3,4.  a 

.       .       .  h 


Pathological 
indicators. 


Microcytes  (small  size) 

Macrocytes  (large  size) 

Megalocytes  (very  large  size)  ......  i 

Poikilocytes  (irregular  form) d  e  f  g 


Erythroblasts  (nucleated  f  r 

red   corpuscles  derived  J  Pathological  J 


from   red   marrow 
bones) 


of  I       indicators. 


Normoblasts  (normal  size) 
Mioroblasts  (small  size) 
l^  Megaloblasts  (large  size)     . 


j  k 


I>eukocytes     (white    cor- 
puscle.s)        .       .       .       . 


Normal  to 
blood. 


Pathological 
indicators. 


See  Plato, 

Fig.  53  Fig.  I 

Lymphocytes  (small) 22%    5  / 

Lymphocytes  (large) 6  "     6  e 

Polymorphonuclear  neutrophiles       .      .    70 "     7  a 

Polymorphonuclear  eosinophiles         .       .      2  "     S  b 

I  Basophilic  leukocytes  or  mast  cells. 

\  Neutrophilic  myelocytes  from  bone-marrow  .      .  c 

[  Eosinopliilic  mvelocytes d 

(113) 


114 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 
Fig.  53 


Normal  blood  (triacid  stain):  1,  normal  red  cell,  flatly  spread  and  evenly  stained; 
2,  normal  rouleau;  3,  normal  red  cells  varying  slightly  in  size,  thickly  spread,  show- 
ing central  clear  areas;  4,  normal  red  cell,  of  slightly  altered  shape;  5,  lymphocyte, 
medium  size;  6,  large  mononuclear  leukocyte,  incurved  nucleus;  7,  polynuclear 
neiitrophile  leukocyte;  8,  eosinophile  leukocyte.  Separate  nuclear  lobes.  (Schmaus 
and  Ewing.) 


ANEMIA. 

Anemia  is  a  condition  in  which  the  blood  is  lessened  in  quantity 
or  partly  deprived  of  its  essential  constituents — i.  e.,  red  corpuscles 
and  hemoglobin — in  consequence  of  which  the  tissues  receive  less 
oxygen  and  the  general  nutrition  is  impaired. 

Acute  Traumatic  Anemia  occurs  as  a  result  of  copious  hemor- 
rhage. The  individual  becomes  temporarily  pale  and  weak.  The 
arterial  pressure  is  lessened,  the  circulation  slowed,  and  the  pulse 
is  frequent  and  small.  Recovery  is,  as  a  rule,  prompt,  the  water 
being  first  restored  and  later  the  corpuscles  being  regenerated.^ 
Frequent  hemorrhages  cause  the  blood  to  become  watery  and  debility 
results  from  impaired  nutrition.     (See  Plate,  Fig.  III.) 

1  Ziegler,  General  Pathology. 


ANEMIA  115 

Symptomatic  Anemia. — A  diminution  in  the  number  of  red  cor- 
puscles may  occur  as  a  result  of  protracted  overwork,  anxiety,  study, 
or  long-continued  illness,  such  as  a  fever. 

The  number  of  red  blood  corpuscles  may  be  reduced  to  one-half  the 
normal  amount,  and  there  is  a  corresponding  debility.  The  condition 
may  disappear  with  appropriate  removal  of  the  cause. 

Chlorosis. — This  is  a  form  of  anemia  occurring,  for  the  most  part, 
in  girls  and  young  women,  and  characterized  by  a  great  deficiency 
in  the  hemoglobin  of  the  red  corpuscles  without  a  corresponding 
reduction  in  the  number  of  the  red  corpuscles.  In  the  watery  blood 
very  small  red  corpuscles  (microcytes)  are  seen;  also  a  few  very 
large  ones  (macrocytes),  and  some  of  irregular  outline  (poikilocytes).^ 
Myelocytes  are  occasionally  seen.  (Stengel.)  The  pathology  is 
uncertain.  If  prolonged,  the  red  corpuscles  may  sink  in  numbers 
to  3,000,000  or  2,000,000  per  cubic  millimeter  and  20  per  cent,  of 
hemoglobin. 

Being,  as  a  rule,  readily  cured  by  a  course  of  iron,  it  is  inferred 
that  the  body  is  starved  of  iron,  an  essential  constituent  of  hemo- 
globin. It  is  often  associated  with  gastric  disturbances,  constipation, 
defective  hygiene,  and  irregular  habits,  which  apparently  have  a 
causal  relation.  The  skin  and  mucous  membranes  are  pale  and  have 
a  slightly  greenish  tinge.-  In  recovery  the  number  of  corpuscles  is 
first  increased,  then  the  hemoglobin. 

Leukocytosis. — This  is  not  a  form  of  anemia,  but  a  temporary 
increase  in  the  number  of  multinucleated  leukocytes,  apparently 
derived  from  the  lymphoid  structures  of  the  body  in  response  to 
some  demand  for  leukocytes.  Thus  it  occurs  after  a  full  meal,  in  the 
later  months  of  pregnancy,  in  acute  fevers,  in  tuberculosis,  and  in 
conditions  accompanied  by  suppuration.^  Its  presence  during  the 
course  of  surgical  disease  has  been  held  to  be  diagnostic  of  pus  forma- 
tion*— e.  g.,  in  abdominal  surgery  from  8000  to  20,000  per  cubic 
millimeter.    (See  Plate,  Fig.  IV.) 

Leukemia. — Leukemia  is  a  disease  characterized  by  a  consider- 
able increase  in  the  number  of  white  corpuscles  of  the  blood,  by  a 
diminution  in  the  number  of  the  red  corpuscles,  and  by  enlargement 
of  some  of  the  lymphatic  organs.  The  proportion  of  one  white  to  ten 
red  corpuscles  is  common  (1  to  5  often,  occasionally  1  to  1).  The 
spleen  may  be  hypertrophied  (splenic  leukemia).  The  lymphatic 
glands  ma}'  be  hypertrophied  (lymphatic  leukemia).  In  these  latter 
cases  the  blood  contains  an  excess  of  uninuclear  leukocytes.    It  is  rare 

^  Green,  Patholoorj'  and  Morl)icl  Anatomy. 

-  Ibid.  '  ^  Ibid. 

*  Cabot,  Boston  Morlioal  and  Siir^ir-al  Journal. 


116  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

except  when  combined  with  other  forms.  When  the  marrow  of  bones 
is  hypertrophied  (myelogenic  leukemia)  large  mononuclear  leukocytes 
with  neutrophile  granules  are  found^  (myelocytes)  and  the  lympho- 
cytes and  polymorphonuclear  forms  are  increased.^  The  blood  con- 
tains toxic  substances  generated  by  the  destruction  of  leukocytes, 
xanthin  bodies,  and  acids  (lactic,  acetic).  The  urine  frequently 
contains  an  excess  of  xanthin  bases  and  lactic  acid.  (See  Plate, 
Figs.  VI  and  VII.) 

Pernicious  Anemia. — This  is  a  comparatively  rare  but  generally 
fatal  disease,  characterized  chiefly  by  a  great  fall  in  the  number  of 
red  corpuscles  to  one  million  or  less  per  cubic  millimeter,  those 
remaining  being  altered  in  form  and  size  and  showing  evidences  of 
degeneration.  The  total  hemoglobin  is  reduced,  but  the  relative 
amount  may  be  increased.  Degeneration  is  shown  by  peculiarities 
of  staining.  Normal  red  corpuscles  (normocytes),  nucleated  red 
corpuscles  (megaloblasts) ,  large  nucleated  red  corpuscles  (giganto- 
blasts),  microcytes,  and  poikilocytes  are  found.  The  blood  platelets 
and  leukocytes  are  somewhat  diminished.^  The  oxygen-carrying 
power  is  markedly  lessened  and  all  tissues  suffer  from  malnutrition. 
The  power  of  coagulation  of  the  blood  is  lessened.  Marked  fatty 
degeneration  of  the  heart  muscles  is  apt  to  occur*  as  well  as  fatty 
changes  in  the  kidneys  and  liver. 

The  causes  are  obscure,  but  gastro-intestinal  disorders,  intestinal 
parasites,  pregnancy  and  lactation,  hemorrhages,  malaria,  syphilis, 
tuberculosis,  and  infections  are  the  chief  causes  supposed  to  produce  it. 

Aplastic  anemia  is  a  severe  type  of  progressive  pernicious  anemia, 
in  which  the  bone-marrow  fails  to  develop  myelocytes  and  erythro- 
blasts  owing  to  lack  of  marrow  cells  (hypoplasia  of  bone-marrow.) 

COAGULATION   OF    THE   BLOOD. 

The  blood  when  drawn  from  the  body  or  in  contact  with  a  wounded 
surface  of  injured  vessel  wall  undergoes  a  process  of  solidification 
called  coagulation.  The  nature  of  the  process  is  in  some  doubt,  but 
it  is  now  thought  that  the  injury  of  white  corpuscles,  blood  platelets 
and  tissue  cells  liberates  a  ferment  called  thrombokinase,  which  with 
the  aid  of  calcium  salts  converts  the  prothrombin  in  the  blood  plasma 
(thrombogen)  into  thrombin.  This  .combines  chemically  with  the 
fibrinogen  of  the  plasma  to  form  fibrin  which  takes  the  form  of  a 

1  Ziegler,  General  Pathology. 

2  Stengel,  A  Text-book  of  Pathology. 

^  Green,  Pathology  and  Morbid  Anatomv. 
'  Ibid. 


COAGULATION  OF   THE  BLOOD 


]]• 


network,  in  the  open  ,si)aees  of  wliieli  tJie  ('()ri)n,scles  are  entaii<;ie(l 
(Fig.  54).^    Coagulation  may  oeenr  in  tlie  li\'ing  vessel,  as  a  throm- 

l)us,  or  in  the   interstitial   tissue, 
i''^^-  ^"^  as  in   inflammation   and   infare- 

tion. 
A    --'i^^T^^^^^^i^^K^  Thrombosis.' — The  formation 

of   thrombi  or  clots  within    the 

Fig.  55 


Fibrin  filaments  and  blood  tablets. 
A,  network  of  fibrin,  shown  after 
washing  away  the  corpuscles  from  a 
preparation  of  blood  that  has  been 
allowed  to  clot;  many  of  the  fila- 
ments radiate  from  small  clumps  of 
blood  tablets;  B  (from  Osier),  blood 
corpuscles  and  elementary  particles 
or  blood  tablets  within  a  small  vein. 


A  thrombus  in  the  saphenous  vein, 
showing  the  projection  of  the  conical 
end  of  the  thrombus  into  the  femor.-d 
vessel:  S,  saphenous  vein;  T,  throm- 
bus; C,  conical  end  projecting  into 
femoral  vein.  At  v,  v,  opposite  the 
valves,  the  thrombus  is  softened. 
(Virchow.) 


Diagram  to  show  phenomena  of 
venous  thrombosis:  v,  v,  valves  of  veins; 
a,  b,  primary  thrombus  (white) ;  c,  d, 
e,  /,  g,  secondary  white  thrombi  con- 
nected with  primary  white  thrombus 
by  various  red  thrombi;  h,  piece  of  white 
thrombus  becoming  detached  by  blood 
current.     (Green,  modified  from  Thoma.) 


living  vessel  may  occur  in  the  heart,  arteries,  veins,  or  capillaries.  If 
the  blood  stream  be  somewhat  retarded,  an  increased  number  of 
white  corpuscles  and  blood  platelets  occupy  the  peripheral  zone  and 

^  Howell,  Text-book  of  Physiology. 


118 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


adhere  to  the  vessel  wall  If  the  vessel  wall  be  injured,  the  blood 
platelets  become  attached  to  it.  With  these  platelets  the  white 
corpuscles  and  sometimes  the  red  become  deposited.  Fibrin  forms 
and  the  corpuscles  are  included.  The  thrombus  is  red  when  red 
corpuscles  are  included  in  it;  white  when  only  white  corpuscles  are 
present.  The  causes  of  thrombosis  are  these:  (1)  a  retardation  of 
the  blood  current  at  some  point  from  some  cause;  (2)  local  changes 
in  the  walls  of  the  vessels  and  (3)  probably  pathological  changes  in 
the  blood. ^ 


Fig.  57 


Fig.  58 


Embolus  impacted  at  the  bifurcation 
of  a  branch  of  the  pulmonary  artery, 
showing  the  formation  of  thrombi  be- 
hind and  in  front  of  it,  and  the  exten- 
sion of  these  as  far  as  the  entrance  of  the 
next  collateral  vessels:  £',  embolus;  t, 
t',  secondary  thrombi.     (Virchow.) 


Diagram  of  a  hemorrhagic  infarct: 
ft,  artery  obliterated  by  an  embolus  (e) ; 
V,  vein  filled  with  a  secondary  throm- 
bus (th) ;  1 ,  centre  of  infarct  which  is 
becoming  disintegrated;  2,  area  of 
extravasation;  3,  area  of  collateral  hy- 
peremia.    (O.  Weber.) 


Older  thrombi  are  firmer  than  those  recently  formed.  Thrombi 
are  also  formed  in  the  capillaries,  a  circumstance  which  favors  the 
spontaneous  cessation  of  hemorrhage.  They  may  form  in  the  vessels 
in  inflammation.  Remaining  in  the  situations,  in  which  they  were 
formed,  they  either  undergo  simple  or  puriform  softening  or  are 
calcified,  or  are  resorbed  and  replaced  by  connective  tissue.  (See 
Regeneration.)  The  calcified  varieties  are  called  phleboliths  in  the 
veins;  arterioliths  in  the  arteries.  In  senile  gangrene  a  thrombus 
may  extend  a  great  distance. 

Embolism. — Portions  of  the  softened  varieties  of  thrombi  may 
become  detached  and  float  about  in  the  blood;  these  are  called 
emboli.  Other  foreign  substances  may  act  as  emboli — e.  g.,  air  or 
fat  globules.  In  important  p^arts  it  may  cause  local  anemia,  necrosis, 
or  slow  or  rapid  death. 


1  Ziegler,  General  Pathology. 


COAGULATION  OF   THE  BLOOD  119 

If  the  thr()ni])us  be  septic,  as  in  the  case  of  purifonn  softening,  the 
emboH  may  lodge  in  small  vessels  and  cause  secondary  septic  disease 
processes,  as,  for  example,  in  the  cases  of  pyemia  accompanied  by 
infarctions. 

Infarction. — When  an  embolus  occludes  a  terminal  artery,  that 
is,  an  artery  whose  branches  spread  like  those  of  a  tree  without 
anastomosis,  the  part  first  becomes  ischemic,  but  soon  the  backward 
pressure  from  the  vein  upon  the  blood  in  the  capillaries  causes  an 
extravasation  of  blood  into  the  interstitial  tissue  of  the  wedge-shaped 
area,  forming  what  is  called  a  hemorrhagic  infarct.  A  clot  forms, 
degeneration  of  the  clot  occurs,  and  if  aseptic  it  is  absorbed  and 
replaced  by  connective  tissue  (see  Regeneration);  if  caused  by  a 
septic  embolus,  it  may  be  involved  in  the  resulting  septic  process — 
e.  g.,  in  pyemic  metastatic  abscess.  Infarcation  has  been  held  by 
Black  to  occur  in  the*  dental  pulp.  A  demonstration  has  been  made 
by  Hopewell-Smith.    (See  Diseases  of  the  Pulp.)     (See  Fig.  58.) 

Hemorrhage. — By  hemorrhage  is  meant  the  escape  of  blood  from 
the  vessels.  It  may  be  arterial,  venous,  or  capillary.  If  the  vessel 
is  ruptured,  it  is  hemorrhage  hy  rhexis.  If  it  occurs  by  diapedesis, 
as  in  infarction  (from  veins  and  capillaries  only),  it  is  hemorrhage 
hy  diapedesis.  The  diapedesis  occurs  through  the  capillary  wall 
rather  than  the  stomata;  pressure  is  the  cause.  Hemorrhage  usually 
ceases  spontaneously  through  thrombosis. 

If  hemorrhage  occurs  into  the  tissues  it  receives  the  following 
designations,  the  escape  itself  being  called  an  effusion  or  extrava- 
sation : 

Ecchymosis,  an  effusion  of  moderate  extent  into  tissue  beneath  a 
surface,  as  into  subcutaneous  tissue. 

Petechia  the  same,  but  small  and  circumscribed ;  when  an  extensive 
area  is  involved  it  is  termed  a  suffusion. 

Infarction,  when  the  area  involved  is  that  supplied  by  terminal 
and  non-anastomosing  arteries. 

Hemorrhage  involves  an  injury  to  vessels  by  traumatism,  or 
disease  rendering  them  incapable  of  retaining  the  blood,  or  by 
increased  pressure,  as  in  violent  exertion,  or  in  congestion  of  local 
vessels,  as  in  venous  hyperemia,  or  as  the  result  of  diminished 
atmospheric  pressure,  as  in  high  altitudes.  The  extravasated  blood 
corpuscles  may  be  disintegrated  into  pigments  (see  p.  88),  and  be 
absorbed  or  deposited  in  the  tissues,  as  in  a  bruise;  or  excite  inflam- 
mation or  cyst  formation  (extravasation  cyst).  Acute  hemorrhages 
or  repeated  extravasations  lead  to  anemia  (which  see). 

Hemorrhagic  Diathesis. — This  is  a  condition,  largely  hereditary, 
in  which  coagulation  does  not  close  wounds  readily,  and  ordinarily 


120  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

trivial  wounds  may,  in  spite  of  surgical  aid,  induce  death  by  hemor- 
rhage. Hereditary  hemorrhagic  diatheses  (hemophilia)  is  usually 
transmitted  through  the  female  to  the  male  descendants — /.  e.,  from 
grandfather  to  grandson  through  the  grandfather's  daughter — and 
seven  or  more  generations  of  hemophiliacs  have  been  recorded.^ 
Males  suffer  more  than  females  in  the  ratio  of  about  11  to  1 . 

In  a  family  of  207  members,  in  four  generations,  37  were  hemo- 
philics, all  of  the  male  sex;  almost  half  died  from  hemorrhages, 
usually  in  infancy,  while  the  tendency  to  bleed  lessened  as  they 
grew  older.2 

According  to  Legg,'^  "It  is  of  three  degrees  of  severity: 

"1.  Characterized  by  external  and  internal  bleedings  of  every 
kind,  and  by  joint  affections. 

"2.  By  spontaneous  hemorrhages  from  mucous  membranes,  but 
no  traumatic  bleeding  or  ecch^ymoses,  and  no  joint  affections. 

"3.  A  tendency  simply  to  ecchymoses.  The  first  seen  most 
frequently  in  men,  the  second  in  women;  the  third  may  appear 
in  either  sex." 

The  joint  affections  are  due  to  hemorrhage,  and  simulate  rheumatic 
affections.  Hemophiliacs  are  apt  to  be  thin-skinned,  neurasthenic, 
and  liable  to  sudden  flushings  and  vasomotor  disturbances.^  Blondes 
suffer  more  than  brunettes.^ 

The  injured  part  may  bleed  from  the  first,  or  a  normal  clot  may 
form  and  secondary  hemorrhage  or  capillary  oozing  occur.  Death 
may  rapidly  occur,  or  the  patient  bleed  to  fainting  or  until  almost 
dead,  and  hemorrhage  then  cease.  This  may  require  any  period, 
even  weeks.    One  case  is  said  to  have  continued  for  a  year.® 

The  pathology  of  the  condition  is  uncertain.  Fillebrown'^  reports 
a  fatal  case  in  which  the  arteries  were  excessively  thin.  Porter  points 
out  that  the  blood  may  clot  in  the  receptacle,  yet  not  in  the  small 
vessels  of  the  wound,  and  infers  that  some  hereditary  deficiency  exists 
which  interferes  with  the  action  of  the  vasoconstrictors. 

Hemophilics  usually  manifest  a  history  of  bleeding  before  puberty, 
and  hemophilic  infants  have  died  from  hemorrhage  due  to  gum- 
lancing,  circumcision,  etc.  Certain  surgical  cases  in  which  secondary 
hemorrhages  have  been  due  to  the  action  of  the  continuous  use  of 
acetanilid  have  been  reported.  The  therapeutic  measures  indicated 
are  hemostatics  internally,  local  styptics,  compresses,  etc.  Potassium 
permanganate,  made  into  a  paste  with  vaselin,  is  recommended  as  a 

1  Porter,  International  Dental  Journal,  1900. 

2  Losser,  International  Journal  of  Surgery. 

3  Musser,  Medical  Diagnosis.  *'  Porter,  Loc.  cit. 

5  Thompson,  Practical  Medicine.  "  Scott,  Dental  Cosmos,  1912,  p.  60. 

^  International  Dental  Journal,  1900. 


COAGULATION  OF   THE  BLOOD  121 

styptic.  A  solution  of  calcium  clilorid,  <;r.  xxx,  and  water,  5.),  lici« 
been  used  on  cotton  with  satisfaction. 

In  case  of  tooth  extraction  reimplantation  has  been  urged,  but 
must  be  done  under  aseptic  precaution,  as  any  infected  dead  pulp  or 
even  a  root  infected  by  contact  with  the  hands,  saliva,  etc.,  may 
substitute  a  condition  almost  as  bad  as  the  hemorrhage. 

In  a  severe  hemorrhage  upon  the  palate,  as  after  lancing  an 
abscess,  finger  pressure  ma}'  be  used,  or,  if  necessary,  a  vulcanite 
plate  may  be  made  to  produce  the  necessary  pressure.^ 

Sodium  sulphate,  gr.  iss,  every  two  hours,  has  been  of  service  in 
marked  hemorrhages.^ 

The  following  is  useful: 

I^ — Calcii  chloridi gr.  Ixxv  to  cl 

Syrupi  menthse 3v 

Aquae  destillatse fgiiiss — M. 

Tablespoonful  doses  or  a  clyster  containing  75  grains  calcium  chlorid  and  a  few 
drops  of  tincture  of  opium. ' 

For  persistent  postextraction  hemorrhage,  Endelmann  has  recom- 
mended : 

I^— Vini  ergots,  U.  S fgij 

Sig. — Teaspoonful  every  two  hours. 

Dilute  sulphuric  acid  and  hydrastis  canadensis  are  used,  also 
gelatin  locally  and  by  injection.^  The  gelatin  may  contain  tetanus 
spores  and  should  be  sterilized  for  forty  minutes  or  longer  at  100°  or 
120°  C.''  Suprarenal  extract,  gr.  xx  to  5j-  topically,  gr.  x  by  mouth, 
every  four  hours,  is  also  useful.  Absolute  quiet  and  the  withholding 
of  food  for  two  days;  the  hunger  to  be  relieved  by  small  doses  of 
opium  and  thirst  by  iced  water  in  small  quantities.^  The  acute 
anemia  induced  requires  treatment. 

Individuals  known  to  be  hemophilic  should  live  a  hygienic  life  and 
avoid  all  injuries,  however  slight,  possible  to  avoid,  in  the  hope  of  an 
eventual  outgrowing  of  the  condition.  If  operation  be  unavoidable, 
they  should  be  treated  with  calcium  chlorid,  gr.  iij  ter  in  die,  for  not 
more  than  four  days,  as  thereafter  the  coagulability  of  the  blood  is 
decreased.'^  Much  larger  doses,  gr.  xxx  to  §  j,  have  been  satisfactorily 
given  for  cure  and  prevention.^  Scott  states  three  cases  in  which 
it  was  of  no  value,  and  suggests  strontium  lactate  15 -grain  dose  to 
be  used  by  the  patient.     Calcium  lactate,  first  dose  20  grains,  five 

1  Joly,  see  Dental  Cosmos,  1909,  p.  488. 

2  Reverdin,  Dental  Cosmos,  February,  1904,  p.  162. 

5  Rosod,  New  York  Medical  Journal.  ''  Hare,  Practical  Therapeutics. 

5  Journal  American  Medical  Association.  ^  Porter,  loc.  cit. 

^  Hare,  loc.  cit.  s  See  Dental  Cosmos,  1908,  p.  185. 


122  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

grains  each  hour  thereafter,  increasing  to  20  grains,  was  successfully 
used  by  C.  F.  Jones  in  a  case  lasting  several  weeks.'  P.  Emile  Weil 
has  suggested  the  injection  of  20  c.c.  of  fresh  human,  horse,  or  rabbit 
serum  before  operation,  for  the  prevention  of  hemorrhage  in  hemo- 
philics, or  every  three  months  as  a  curative  measure.^  Dr.  E.  W. 
Scott^  reports  the  use  of  30  c.c.  of  normal  serum  by  large  hypodermic 
syringe  as  immediately  curative  of  a  hemorrhage  lasting  two  and 
a  half  days  after  extraction,  and  20  c.c.  as  curative  in  three  to  four 
hours  in  a  case  of  stab  wound.  Both  were  blacks.  The  back  was 
selected  as  the  site  of  injection.  To  obtain  human  serum  he  sug- 
gests a  willing  volunteer,  not  a  black  or  relative,  a  large  blister  to 
be  raised. 

LOCAL   DISTURBANCES    OF   THE   CIRCULATION. 

The  amount  of  blood  in  a  part  may  be  increased  or  diminished. 
The  types  of  local  disturbance  of  the  circulation  differ  as  to  causes, 
phenomena,  and  effect,  and  as  to  the  indicated  treatment  for  each. 

In  health  the  bloodvessels  are  maintained  at  a  proper  caliber 
through  the  action  of  two  sets  of  vasomotor  nerve  fibers: 

1.  The  vasoconstrictors,  which  control  the  involuntary  muscles 
of  the  vessel  wall,  and  which,  when  stimulated,  cause  contraction  of 
the  vessel. 

2.  The  vasodilators,  which,  when  stimulated,  inhibit  the  musc'ular 
actioi>  and  permit  dilatation. 

Ischemia. — This  is  local  anemia.  The  quantity  of  blood  in  a 
part  is  less  than  normal.  It  is  direct  when  some  cause  obstructs  the 
flow  from  an  artery  into  a  part,  as  when  pressure  of  any  sort  is 
applied  directly  to  a  part  or  to  the  artery  leading  to  it,  or  when  an 
injection  of  fluid  has  been  made  into  a  part,  as  in  cocain  injections. 
Disease  of  an  artery  may  deprive  a  part  of  blood,  as  in  thrombosis 
or  arteriosclerosis.  Anastomotic  circulation  may  eventually  relieve 
a  part;  if  not  it  remains  pale  and  cold,  atrophies,  and  may  undergo 
degeneration  or  necrosis.    An  infarct  may  remain  ischemic. 

Arterial  Hyperemia. — Arterial  or  active  hyperemia  is  a  more  or 
less  prolonged  increase  in  the  amount  of  blood  in  the  dilated  arteries 
of  a  part.  It  expresses  the  reaction  which  occurs  as  the  consequence 
of  the  presence  of  an  irritant,  the  action  of  which  lessens  the  arterial 
tension  and  permits  dilatation  with  a  consequent  excess  of  blood. 

Etiology. — The  lessened  arterial  resistance  is  produced  either  by  a 
stimulation  of  the  vasodilator  nerves  or  a  sedation  or  paralysis  of  the 

1  New  Jersey  Dental  Journal,  October,  1913. 

2  Dental  Cosmos,  1908,  p.  436.  ^  ibid.,  January,  1912. 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION  123 

vasoconstrictor  nerves.  Certain  causes  act  to  produce  constriction  ui 
the  vessels,  but  later  the  muscle  cells  of  the  walls  are  fatigued  and 
dilatation  results — e.  g.,  the  reaction  after  the  prolonged  application 
of  cold. 

The  removal  or  diminution  of  pressure,  to  which  vessels  have 
become  accustomed,  is  also  a  cause  of  their  dilatation;  often  sudden 
enough  to  cause  bursting. 

Irritants  and  mild  injuries  act  upon  the  sensory  nerves  of  a  part, 
and  by  reflex  action  through  the  vasomotors  (sympathetic  system) 
produce  hyperemia  of  the  part  itself — e.  g.,  heat  as  a  cause. 

Irritation  of  sensory  nerves  may  induce  a  reflex  hyperemia  in  other 
parts  to  which  branches  of  the  same  nerve  are  distributed — e.  g.,  the 
peripheral  hyperemia  of  neuralgia,  induced  by.  irritation  of  a  tooth 
pulp. 

A  similar  effect  may  be  produced  in  deep-seated  organs  to  w^hich 
other  nerves  are  distributed — e.  g.,  hyperemia  of  deep  organs  through 
the  application  of  irritants  to  the  skin  over  them  or  hyperemia  of  the 
intestinal  wall  (tenth  nerve)  as  the  result  of  the  stimulation  of  a  pulp 
underlying  an  erupting  tooth  (fifth  nerve). 

Collateral  hyperemia  is  induced  by  the  diminished  flow^  of  blood  to 
other  parts — e.  g.,  by  the  bandaging  of  parts  or  through  the  chilling 
of  the  surface  of  the  body.  A  part  having  a  lessened  resistance  may 
become  hyperemic. 

Compensatory  hyperemia  may  occur  through  the  removal  of  one  of 
a  pair  of  organs;  the  other  receives  the  excess  of  blood,  sometimes 
becomes  hypertrophied,  and  takes  upon  itself  an  increased  amount 
of  work.  (See  Hypertrophy.)  A  physiological  hyperemia  occurs  in 
organs  during  periods  of  activity,  the  work  required  acting  as  a 
stimulus  to  the  vasomotor  nerves. 

Arterial  hyperemia  is  produced  as  the  first  step  in  the  process  of 
inflammation,  but  can  be  independent  of  it.     (See  Inflammation.) 

Pathology. — The  arteries  are  dilated;  there  is  an  increased  flow  of 
blood  through  them  and  also  to  them  through  their  own  nutritive 
arteries;  the  pressure  in  the  veins  rises  as  the  veins  are  enlarged  to 
accommodate  the  blood.  As  exudation  sometimes  does  not  increase 
markedly,  the  lymph  pressure  is  not  increased  except  in  marked 
cases,  in  which  some  edema  may  occur.  The  function  of  the  part 
may  be  disturbed  in  the  more  marked  cases.  (For  illustrations,  see 
Hyperemia  of  the  Pulp.) 

Results. — Continued  arterial  hyperemia,  as  a  rule,  results  in  an 
increase  of  nutrition,  even  to  the  arteries  themselves  via  the  vasa 
vasorum.  Ihe  arteries  may  be  permanently  enlarged,  their  walls 
thickened,  and  the  tissues  about  them  hypertrophied  in  consequence 


124  DISTURBANCES  OF   THE    VASCULAR  SYSTEM 

of  the  increased  capacity  for  work  in  the  part.  Hyperesthesia  of 
nerves  and  nervous  tissue  is  often  a  result.  In  marked  hyperemia 
with  function  altered  there  is  a  tendency  to  the  degenerations. 
(See  Arterial  Hyperemia  of  the  Pulp.) 

Symptoms. — These  naturally  would  be  and  are  increased  redness, 
temperature,  and  sensibility;  more  or  less  throbbing  in  marked  and 
pathological  cases,  in  some  cases  swelling  and  throbbing  pain.  The 
increased  temperature  is  due  to  the  increased  oxidation.    (See  p.  131.) 

Degrees  of  Hyperemia. — It  is  to  be  borne  in  mind  that  the  hyper- 
emia may  be  of  several  grades,  varying  from  a  very  mild  exaltation 
of  function  and  sensation  to  a  distinctly  pathological  condition  with 
altered  function.  The  effects  may  be  constructive  in  character  or 
destructive,  the  former  due  to  the  increased  nutrition,  the  latter  to 
interference  with  it.  (See  Constructive  and  Destructive  Diseases  of 
the  Pulp.) 

Hyperemia  as  a  Resistance  to  Infection. — According  to  Biers  and 
others  the  induction  of  hyperemia  in  an  infected  part  increases  the 
opsonic  power  of  the  excess  blood,  and  therefore  is  antagonistic  of 
infection.  No  doubt  this  is  the  natural  process  in  inflammation.  It 
has  been  occasionally  noticed  that  stimulation,  as  in  the  use  of  a 
capsicum  plaster  in  acute  apical  abscess,  has  produced  resolution. 
Usually  confined  abscessses  are  enlarged  and  not  cured  by  such 
stimulation. 

Therapeutics. — The  principle  underlying  the  treatment  is  to  remove 
the  cause  and  procure  surgical  rest.  The  symptoms,  as  a  rule,  then 
subside  promptly.  It  may  be  that  the  conditions  require  treatment 
irrespective  of  the  cause,  which  may  not  be  determined  or  be  absent, 
the  vessels  being  dilated  as  the  effect  of  a  previously  acting  cause. 
The  effect  aimed  at  is  the  reduction  of  the  dilated  vessels.  This  is 
attempted  at  times  through  the  use  of  drugs;  for  example,  ergot 
stimulates  the  vasoconstrictor  system  and  lessens  the  caliber  of  all 
the  vessels,  including  those  affected.  Aconite,  the  antagonist  of 
ergot,  reduces  the  heart  action  by  sedating  the  motor  apparatus 
of  the  heart,  thus  reducing  the  arterial  pressure.^  Less  blood  is 
delivered  to  a  part  in  a  given  time.  Many  cases  of  superficially 
seated  hyperemia  are  amenable  to  local  treatment. 

Local  sedation  of  sensory  nerves  and  contraction  of  vessels  are  pro- 
duced by  application  of  dry  or  wet  cold  (ice  bags,  ice  wrapped  in 
muslin,  cloths  taken  in  succession  from  a  block  of  ice,  the  Leiter 
coil,  etc.);  also  by  the  application  of  sedative  astringents,  as  the 
liquor  plumbi  subacetatis  in  the  well-known  formula  of  lead-water 
and  laudanum: 

1  Biddle,  Materia  Medica  and  Therapeutics. 


LOCAL  DISTURBANCES  OF  THE  CIRCULATION 


125 


I^ — Tincturse  opii f5,i 

Liq.  plumbi  subacetatis f§j 

AquiB Oj— M. 

in  which  to  the  astringent  effect  of  the  lead  is  added  the  sedative 
effect  of  the  opium;  if  cold  sedation  and  contraction  are  added. 

The  principle  of  derivation  is  also  employed.  What  is  known  as 
counterirritation  is  a  common  means  of  treatment.  An  irritant  such 
as  a  mustard  plaster  or  a  blister  or  dry  cup  applied  at  a  distance  to 
the  affected  part  induces  a  flow  of  blood  to  the  point  of  application 
and  lessens  the  amount  of  blood  in  the  area  of  hyperemia.  The 
volume  of  the  blood  being  in  definite  amount,  if  an  excess  exists 
in  any  part  a  deficiency  will  be  found  in  other  parts. 

The  hot  pediluvium  acts  upon  this  principle  by  drawing  a  con- 
siderable excess  of  blood  into  the  vessels  of  the  lower  extremities. 
This  action  is  increased  by  add- 
ing  a   small    quantity    (two    or  ^^^'-  ^^ 
three  tablespoonfuls)  of  mustard 
to  the    hot    water.     It    is    sug-              f    j- 
gested  by  Endelmann  that  the             v^ilfepoJ^^^^' 
water  be  at  first  only  warm  and            Jf   )itj   fp£^C?i[ 
the  hot  water  added  as  the  ves-         /^^^M/C/\r  "Q 
sels  relax. ^                                              ("^'rlffCz-w'^'^'' 

The  volume  of  the  blood  may  ^^^1  CjfV''  A.  O    ( 

be  actually  reduced  and  a  deriva-  / 

tive     hyperemia    of    the    sweat 
glands  be  produced  by  the  use  of         ^,  ,  •      r  x,     ,-         t- 

'^.  /  /-I      1  •  Venous  hyperemia  of  the  hver.      iwo 

diaphoretics.       Cathartics     lessen       capillaries    near     central     hepatic     vein, 
the  blood  volume  and  cause  mild       showing  the  thickening  of  the  walls  and 

the  accumulation  of  red  blood  corpuscles 

hyperemia     of    the    alimentary     within  them,     x  500.    (Green.) 
canal.    Diuretics  act  in  a  similar 

way  upon  the  kidneys.     In  deep-seated  hyperemia  counterirritation 
is   valuable   alone   or   conjoined   with   other   forms   of   derivation. 

Venous  Hyperemia. — Venous  (mechanical  or  passive)  hyperemia 
is  an  excess  of  blood  in  a  part  beginning  in  the  veins,  which  are 
dilated  in  the  hyperemic  area,  though  they  may  be  occluded  between 
it  and  the  heart. 

Etiology. — 1.  Any  mechanical  interference  with  the  passage  of  the 
blood  through  the  veins  on  its  way  to  the  heart — e.  g.,  the  action  of 
bandages,  tumors  pressing  on  veins,  thrombi  in  veins,  etc. 

2.  Insufficiency  of  any  of  the  mechanical  forces  aiding  the  pro- 
pulsion of  the  blood  through  the  veins — e.  g.,  diminished  cardiac 
power  or  valvular  insufficiency;  obstructions,  dilatations,  or  rigidity 

1  Dental  Cosmos,  1904. 


126  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

of  arteries;  insufficient  muscular  contraction  upon  or  valvular 
incompetency  in  veins,  or  lessened  or  excessive  thoracic  aspira- 
tion, etc.  The  second  class  of  causes  produces  a  collection  of  blood 
in  the  veins  and  a  consequent  reduction  of  volume  in  the  arterial 
system. 

Pathology. — The  veins  are  dilated,  the  current  is  slowed,  and  the 
intravenous  pressure  is  increased,  in  consequence  of  which  watery 
(serous)  exudations  occur  in  the  parts  about  them  (edema).  For 
the  same  reason  in  marked  cases  diapedesis  of  red  corpuscles  may 
occur  (hemorrhage  by  diapedesis),  and  their  hemoglobin  may  be 
dissolved  out.  The  blood  in  the  parts  not  being  sufficiently  changed, 
and  in  some  cases  in  a  state  of  stasis,  there  is  a  lessened  food  supply 
and  waste  removal,  and  cell  nutrition  suffers  accordingly.  Vital 
processes  are  lessened,  secretion  is  diminished,  there  is  less  oxidation, 
and  hence  less  heat  is  produced  and  less  work  is  done.  Fatty  degener- 
ation, atrophy,  and  in  markedly  continued  cases  necrosis  may  occur. 
Long-continued  venous  hyperemia  with  great  intravenous  pressure 
may  produce  dropsies.  If  the  walls  of  the  veins  are  weak  and 
are  permanently  distended  or  thicken  under  pressure  and  become 
tortuous,  the  condition  is  called  varicosity  of  the  veins  (varicose 
veins).  The  exudate  of  venous  hyperemia  differs  markedly  from 
that  of  inflammation.^ 

Hyperemic  Exudate.  Inflammatory  Exudate. 

Poor  in  albumin.  Rich  in  albumin. 

Rarely  coagulates  in  the  tissue.  Usually  coagulates  in  the  tissue. 

Contains  few  cells.  Contains  numerous  cells. 

Low  specific  gravity.  High  specific  gravity. 

Contains  no  peptone.  Contains  peptone  (product  of  cell 

disintegration) . 

This  is  probably  due  to  an  increased  permeability  in  the  vessel  wall 
in  inflammation  permitting  the  albumin  of  the  blood  to  pass  through. 

Therapeutics. — The  treatment  consists  of  the  removal  of  the  me- 
chanical obstruction  to  the  return  of  the  blood  and  mechanical  sup- 
port of  the  engorged  vessels,  with  a  view  to  recovery  of  the  tone  of 
their  muscular  walls.  This  latter  is  accomplished  by  means  of  elastic 
bandages  or  compresses,  and  in  situations  in  which  these  cannot  be 
used  astringents  may  be  employed.  The  part  is  elevated,  when 
possible,  to  aid  in  the  return  of  the  blood  to  the  heart.  In  certain 
circumstances,  as  in  an  engorged  tooth  pulp,  actual  depletion  of  the 
engorged  part  must  be  resorted  to  by  bloodletting.  (See  Destructive 
Diseases  of  the  Pulp.)  In  cases  due  to  failure  of  blood-propelling 
forces  these  are  to  have  appropriate  treatment. 

1  Park's  Surgery. 


INFLAMMATION  127 

INFLAMMATION. 

Inflammation  may  be  defined  as  a  series  of  hyperemia  changes 
expressive  of  the  reaction  of  Hving  tissue  to  irritation,  and  character- 
ized chiefly  by  an  excessive  diapedesis  of  leukocytes  and  exudation 
of  coagulable  lymph  from  the  bloodvessels. 

Etiology. — Any  irritant  or  injury  capable  of  producing  a  lesion  of 
the  bloodvessel  wall  not  involving  its  immediate  death  can  produce 
inflammation.  In  case  direct  death  is  produced,  the  inflammation, 
if  any,  occurs  in  the  tissue  contiguous  to  the  dead  part. 

The  causes  of  inflammation  may  be  divided  first  into  non-septic 
and  septic  or  infective.  The  non-septic  causes  may  be  extrinsic  or 
intrinsic.  The  extrinsic  non-septic  causes  are:  (1)  Physical  irritants, 
such  as  violence,  mechanical  irritation,  pressure  or  traumatism, 
excessive  heat  or  cold,  and  electrolytic  action.  (2)  Chemical  irri- 
tants— e.  g.,  the  action  of  acids,  caustics,  etc.  (3)  Nervous  or  vital 
irritants — e.  g.,  rubefacients,  epispastics,  arsenic,  etc.  These  act 
only  on  living  tissue  through  the  medium  of  the  nerves. 

An  intrinsic  non-septic  cause  may  produce  inflammation — e.  g., 
urates  in  tissue,  mechanical  strains  upon  tissue,  temporary  laclv  of 
blood  in  a  vessel  or  central  nervous  disturbance,  as  in  herpes  from 
locomotor  ataxia. 

Non-septic  causes,  as  a  rule,  produce  only  such  mild  inflammatory 
phenomena  as  are  concerned  in  circumvallation  of  an  irritant, 
absorption  of  it,  and  in  repair  or  production  of  new  tissue.  No 
pus  is  produced  unless  pyogenic  bacteria  gain  ingress.  This  class 
of  inflammation  is  termed  simple  inflammation. 

Septic  or  Infective  Causes. — These  are  fungi  or  their  products, 
and  the  classes  of  inflammations  produced  are  much  more  severe, 
continuous,  and  destructive  in  their  nature,  and  are  termed  infective 
inflammations. 

Pathology  of  Simple  Inflammation. — If  to  the  web  of  a  frog's  foot 
tincture  of  capsicum  be  applied,  or  if  its  mesentery  be  exposed  to  the 
air,  and  either  be  examined  under  the  microscope  while  the  animal  is 
living,  it  is  noted  that  after  a  possible  short  period  of  contraction  of 
the  arterioles  dilatation  of  arteries  at  once  begins  and  is  gradually 
followed  by  dilatation  of  the  veins  and  capillaries.  This  continues 
to  steadily  increase  for  about  twelve  hours.  During  the  first  hour 
of  this  period  the  blood  current  is  accelerated  and  the  first  stage 
of  an  inflammation  is  thus  an  aHerial  hyperemia.  Following  this 
acceleration  the  blood  flow  is  increasingly  retarded.  The  retardation 
is  due  to  the  action  of  the  leukocytes,  large  numbers  of  the  mono- 
nuclear and  polymorphonuclear  forms  of  which  fall  out  of  the  central 


128 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


blood  stream  into  the  periaxial  stream  and  collect  along  the  walls  of 
the  small  veins  (Fig.  60,  h).  Several  layers  of  leukocytes  may  thus 
form.  Probably  some  peculiar  attraction  exists  between  the  leuko- 
cytes and  the  wall  of  the  vessel,  or  a  positive  chemotaxis  exists  as  in 
infective  inflammation. 

This  massing  of  leukocytes  compels  the  red  corpuscles  to  the 
centre  of  the  stream  (Fig.  60,  a),  and  their  passage  is  mechanically 
interfered  with;  thus  the  further  dilatation  of  the  vessel  becomes 
a  process  of  venous  hyperemia.  The  vessels  are  increased  in  size 
and  length  and  become  more  tortuous.    Pulsation  is  noted. 


Fig.  60 


--/y 


Small  vein  in  mesentery  of  dog,  after  exposure  for  half  an  hour  and  irrigation  with 
salt  solution :  a,  red  corpuscles ;  6,  leukocytes  adhering  to  wall  of  vein;  c,  red  corpuscles; 
d,  leukocytes  which  have  escaped  from  vessel;  e,  leukocyte  in  act  of  escaping;  /, 
fibrous  tissue.      X  340.     Modified  from  Thoma.      (Green.) 


Coincident  with  retardation  of  the  blood  flow,  the  leukocytes  are 
seen  to  work  their  way  by  an  ameboid  movement  through  the  walls 
of  the  veins  and  to  some  extent  of  the  capillaries  into  the  perivascular 
spaces — i.  e.,  into  the  adjoining  tissue — in  which  they  may  move  far 
from  their  point  of  escape  and  mass  about  the  irritant  if  one  be 
present.  This  process  is  called  emigration  (Fig.  60,  e).  At  the  same 
time  a  fluid  rich  in  albumin,  and  thus  capable  of  coagulation,  escapes 
by  the  same  route  into  the  tissue  (Fig.  61).  Some  red  corpuscles 
also  escape  through  the  walls  (diapedesis)  (Fig.  60,  c).  (While 
inflammation  involves  an  arterial  hyperemia  as  its  first  stage  and 


INFLAMMATION  129 

a  venous  hyperemia  as  its  second  stage,  these  two  conditions  are 
not  necessarily  inflammation,  and  may  exist  as  entirely  distinct 
conditions  when  produced  by  causes  not  leading  to  inflammation; 
also,  it  must  be  remembered  that  the  results  of  venous  hyperemia 
or  infarction,  e.  g.,  extravasation,  may  lead  to  a  subsequent  inflam- 
mation.   This  does  not  make  them  identical.) 

As  the  venous  hyperemia  of  the  inflammation  increases,  the  flow 
of  red  corpuscles  in  the  veins  is  increasingly  retarded  until  stopped, 
when  a  to-and-fro  motion  (oscillation)  begins.  Finally  all  motion 
ceases,  diapedesis  ceases,  and  stasis  is  complete.  This  blood  may 
remain  fluid  in  the  vessel  for  several  days  {i.  e.,  without  coagulation), 
and  if  the  blood  flow  be  reestablished  the  separate  red  corpuscles  are 
seen  one  by  one  to  roll  away  from  the  general  mass  until  all  are  in 
movement  and  stasis  ceases.     (Thoma.) 

Coagulation  (thrombosis)  may,  however,  occur  in  the  vessels 
involved  in  the  stasis,  and  the  part  be  later  removed  through  the 
process  of  resorption.  (See  Resorption  of  Clot.)  With  the  inflam- 
mation fully  established  there  are  in  the  tissue  the  following  elements : 
(1)  Leukocytes  and  some  red  corpuscles  and  lymphocytes  from  the 
tissue  lymphatics.  (2)  Coagulable  lymph.  (3)  Later  new  embryonic 
cells  formed  by  mitosis  from  preexisting  connective-tissue  cells 
which  surround  the  leukocytes  massed  about  the  irritant.  These 
are  fibroblasts  ready  to  form  scar  tissue — i.  e.,  they  are  the  elements 
composing  granulation  tissue. 

The  disposition  of  these  elements  of  inflammation  is  as  follows: 
The  leukocytes  mass  about  the  irritant,  exert  a  certain  amount  of 
phagocytic     activity     (ferment    action), 
and  may  in  turn  be    injured,  liberating  Fig-  61 

fibrin  ferment,  which,  acting  upon  the 
fibrinogen  of  the  lymph,  produces  fibrin, 
which  in  turn  forms  a  coagulum.  This 
coagulum  blocks  the  lymphatic  vessels 
leading  from  the  part  involved,  thus 
causing  a  retention  of  fluid  in  the  tissue. 

Li  the  later  stages  of  non-infective  in- 
flammation the  tissue  cells  undergo  multi-  inflammatory  edema  of  skin. 

'^  .  1  he  large   spaces  shown   were 

plication,  forming  cells  larger  and  having     filled  with  exuded  fluid,     x 
more  power  of  ameboid  movement  and     ^•^"    (J^^y^) 
phagocytosis  than  the  leukocytes.    These 

become  mingled  wnth  the  leukocytes  in  the  area  of  inflammation. 
They  are  fibroblasts  from  which  all  the  connective  tissues  develop, 
and  to  the  action  of  which  regeneration  is  mainly  due.  Around  and 
about  the  focus  of  inflammation  the  bloodvessels  are  in  a  condition 
9 


130 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


of  arterial  hyperemia,  and  about  this  is  an  area  of  normal  tissue. 
These  areas  shade  off  into  each  other.^  The  phagocytes  cause  disso- 
lution of  coagula  and  dead  aseptic  tissue,  and  remove  them.  If  the 
irritant  be  thus  removable  it  is  eaten  away.  If  the  dead  tissue  be 
superficial,  the  connection  with  the  living  tissue  beneath  is  eaten 
through  and  the  latter  thrown  off.  If  the  superficial  tissues  have 
been  previously  removed,  the  wound  is  covered  with  the  exudates 
and  leukocytes,  which  dry  into  a  scab,  beneath  which  regeneration 
occurs.    If  inflammation  occur  in  a  mucous  surface,  the  exudate  and 

Fig.  62 


Acute  bronchial  catarrh:   Passage  of  leukocytes  through  the  epitheHum  of  the  bronchus 
between  the  cihated  cells.      X  700.     (Thoma.) 


corpuscles  escape  from  the  submucous  tissue  between  the  epithelial 
cells  as  a  catarrhal  discharge  (Fig.  62) .  If  the  inflammatory  exudate 
be  highly  coagulable  and  coagulate,  firm  swelling  is  caused,  apt  to 
lead  to  organization  of  tissue,  hence  called  fibrinous  inflammation. 
If  it  be  productive  of  hypertrophy,  it  is  called  productive  inflamma- 
tion.    If  the  exudate  be  watery,  poor  in  albumin,  and  hence  not 

1  Fig.  64  serves  to  illustrate  these  areas,  excepting  the  fact  that  the  central  area  of 
pus  is  absent  and  occupied  entirely  by  an  area  there  termed  lesser  inflammation — i.  e., 
translate  lesser  inflammation  into  simple  inflammation. 


INFLAMMATION  131 

readily  coagulable,  the  inflammation  is  called  serous  inflammation. 
In  the  later  stages  of  simple  inflammation  the  coagula  are  dissolved, 
the  leukocytes  undergo  fatty  degeneration,  and  both  are  absorbed, 
together  with  such  tissue  as  has  undergone  liquefaction.  The  lym- 
phocytes and  embryonic  cells  push  into  the  area  and  regenerate  the 
tissue.  This  is  the  phenomenon  of  resolution. 
Symptoms  of  Simple  Inflammation. — These  are: 

1.  Redness  due  to  the  excess  of  blood  in  the  vessels  and  in  the  tissue. 
In  some  cases  the  part  may  have  a  dusky  hue.  The  color  is  deepest 
in  the  area  of  greatest  stasis. 

2.  Heat  due  to  the  increased  oxidation  in  the  area  of  hyperemia 
about  the  area  of  stasis.  It  has  been  shown  that  there  is  no  increased 
heat  in  the  area  of  stasis.    In  this  area  chemical  action  is  lessened. 

3.  Swelling  due  to  the  excess  of  blood  in  the  vessels,  the  exudates 
of  leukocytes  and  fluid,  and  the  multiplication  of  tissue  cells.  The 
hardness  of  a  swelling  is  due  to  coagulation  of  the  fluid  exudate. 

4.  Pain. — The  result  of  the  pressure  of  the  effusion  upon  sensory 
nerve  terminals;  it  is  frequently  throbbing  in  correspondence  with  the 
heart  beat;  the  impulse  causes  temporarily  increased  pressure  upon 
the  nerve  terminals.  Gravitation  also  increases  the  pressure  and 
pain  in  a  dependent  part — e.  g.,  in  a  hand  or  foot  or  in  recumbency 
in  case  of  pulpitis  (which  see). 

5.  ImjMired  function  is  an  evident  result  of  a  disturbance  involving 
such  pathological  phenomena  as  have  been  described.  The  part 
cannot  be  used  owing  to  pain  and  stiffness  due  to  the  swelling,  also 
nutrition  of  any  part  being  impaired,  it  loses  its  normal  function. 

There  are  no  general  disturbances  in  simple  inflammation  beyond  a 
slight  traumatic  fever  due  to  absorption  of  some  aseptic  material 
from  the  seat  of  inflammation — e.  g.,  fibrin  ferment.^  There  may, 
however,  be  general  disturbance  due  to  pain,  loss  of  sleep,  appetite, 
etc.  Shock  due  to  widespread  inflammation,  as  from  burns,  may  be 
serious. 

Infective  Inflammation.  —  If  microorganisms  enter  the  tissue 
through  a  wound  or  puncture  or  an  abraded  surface,  or  if  they  locate 
upon  predisposed  or  non-resistant  mucous  membrane,  their  multi- 
plication causes  irritation  and  inflammation  of  the  tissue  about  them. 
This  at  first  resembles  a  simple  inflammation,  but  later  becomes 
more  severe,  prolonged,  and  may  spread  into  the  surrounding  tissue, 
or  in  some  cases  cause  inflammation  in  another  place  in  no  way 
connected  with  it  except  by  the  blood  or  lymphatic  channels  (metas- 
tasis).    Briefly  the  process  may  be  described  as  beginning  with  the 

'  Green's  Pathology  and  Morbid  Anatomy. 


132  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

entrance  or  location  of  the  organisms  and  their  multiphcation.  An 
injury  of  the  vessel  walls  and  degeneration  of  some  tissue  occur 
and  the  phenomena,  such  as  occur  in  simple  inflammation,  begin. 
There  is  arterial  hyperemia,  later  retardation  of  the  blood  current; 
diapedesis  of  leukocytes  occurs,  and  a  copious  exudate  of  coagulable 
lymph  is  poured  out  into  the  intravascular  tissue.  By  positive 
chemotaxis  the  leukocytes  are  attracted  to  the  bacteria,  surround 
them,  and  apparently  endeavor  to  limit  their  activity,  or,  perhaps,  to 
digest  them.  If  the  bacteria  be  few  in  number  and  not  too  virulent, 
the  phagocytes  are  successful  and  the  phenomena  of  resolution  occur. 
If,  however,  the  contrary  be  the  case,  the  leukocytes  are  overcome 
and  the  inflammation  spreads.  In  case  of  much  toxin  formation, 
negative  chemotaxis  occurs  and  phagocytic  phenomena  are  held  in 
abeyance.  The  central  or  most  involved  area  dies.  It  is  thus  seen 
that  there  may  be  two  terminations  of  an  infective  inflammation — 
resolution  and  necrosis. 

Resolution. — If  the  phagocytes  destroy  or  wall  up  the  bacteria, 
so  that  they  die  in  their  own  products  or  are  killed  by  the  protective 
juices  of  the  part  (alexins),  the  phagocytes  undergo  fatty  degenera- 
tion, the  lymphatics  are  unblocked,  the  circulation  is  reestablished, 
the  tissue  that  has  died  is  removed  by  resorption  and  replaced  by 
scar  tissue  if  the  loss  be  considerable.  No  evident  pus  or  externally 
evident  necrosis  is  produced,  and  the  part  exhibits  phenomena  much 
like  those  of  a  simple  inflammation.  This  is  the  only  termination 
for  a  simple  (non-infective)  inflammation. 

Necrosis. — Death  of  a  part  may  result  from  infective  inflamma- 
tion, either  with  or  without  pus  formation. 

Suppuration. — If  the  irritant  in  the  tissue  consists  of  pyogenic 
organisms,  such  as  the  Staphylococcus  pyogenes  aureus  or  albus,  the 
Streptococcus  pyogenes,  the  Bacillus  pyocyaneus.  Bacillus  typhi 
abdominalis.  Bacterium  pneumoniae,  or  the  gonococcus,  pus  will 
be  formed,  provided  the  germs  be  not  killed.  The  Staphylococcus 
pyogenes  aureus  is  most  frequently  the  organism  infecting  wounds. 
It  is  practically  universal. 

Entering  a  part,  the  bacteria  distributed  in  the  tissue  act  as  irritants 
and  excite  the  phenomena  of  inflammation  as  described.  Some  of 
the  cocci  are  taken  up  by  the  fixed  connective-tissue  corpuscles,  the 
leukocytes,  and  the  endothelial  cells  of  the  capillaries,  and  some  lie 
free  in  the  tissue.  The  cocci  multiply  and  the  polymorphonuclear  and 
eosinophile  leukocytes  increase  in  number  by  diapedesis  and  surround 
them.  The  original  tissue  cells,  including  those  of  the  bloodvessels, 
undergo  coagulation  necrosis  as  the  result  of  the  action  of  bacterial 
ferments  and  do  not  take  up  staining  reagents  (Fig.  63) .    Coagulation 


INFLAMMATION 


133 


of  the  exudates  oceurs.     The  leukocytes  and  tissue  ceHs  are  in  part 
degenerated  into  pus  corpuscles  by  the  action  of  the  unorganized 


Fig.  63 


Miliary  abscess  in  a  case  of  septic  embolism  of  the  kidney:  a,  leukocytes  advancing 
toward  and  surrounding  (6)  a  mass  of  cocci,  in  whose  neighborhood  all  trace  of  struc- 
ture has  disappeared;  c,  renal  epithelium  too  damaged  by  bacterial  products  to  take 
the  stain;  d,  kidney  tissue  staining  normally;  e,  vein  from  which  leukocytes  are 
making  their  way  to  the  commencing  abscess.      X  100.     (Green.) 


ferments  of  the  bacteria — i.  e.,  their  nuclei  are  fragmented,  and  they 
undergo  fatty  degeneration.     Some  cocci  die.     The  exudate  is  pep- 


134 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


tonized  into  a  fluid,  which,  together  with  the  cocci,  dead  leukocytes, 
and  tissue  remnants,  constitutes  pus.  AV)out  this  pus  is  a  circum- 
vallating  wall  of  living  leukocytes,  and  about  this  again  a  zone  of 
fibroblasts  arranged  about  new  capillary  loops  (granulation  tissue). 
The  whole  constitutes,  when  confined  within  tissue,  an  abscess. 
When  upon  a  surface  the  granulation  tissue  is  upon  the  under  side 
onl}^,  the  whole  constitutes  a  suppurating  ulcer. 


An  abscess  in  the  skin.  The  horny  layer  has  largely  disappeared,  and  the  Malpig- 
hian  layer  is  pushed  upward  by  the  subjacent  abscess  (a).  The  mass  of  pus  corpuscles 
is  just  breaking  down  to  form  a  cavity  (P),  the  walls  of  which  are  thickly  infiltrated 
with  similar  cells  or  the  area  of  stasis  (<S).  Outside  is  the  area  of  lesser  inflammation 
(LI),  and  still  farther  away  are  the  areas  of  arterial  hyperemia  (H)  and  normality 
(N.T).    Interpretation  modified  by  editor.     (Boyd.) 


While  the  leukocytes  may  overcome  the  bacteria,  the  reverse  is 
often  the  case,  and  the  pus  cavity  enlarges  in  the  same  manner  as  at 
first  by  a  new  formation  of  coagulation  necrosis,  more  circumvallation, 
further  liquefaction  of  the  coagulum,  etc.  The  path  offering  the  least 
vital  or  mechanical  resistance  is  usually  followed  until  the  surface  of 
the  body  or  some  internal  cavity  is  reached.  The  last  portion  of 
tissue  overlying  the  forming  pus  is  tumefied  and  a  soft,  yellow  spot 
appears.  This  is  called  pointing.  The  tissue  is  ruptured  by  the 
internal  pressure  and  the  pus  escapes.  The  tract  from  the  point  to  the 
abscess  cavity  is  a.  fistula  or  sinus.  As  soon  as  this  occurs  granulation^ 
tissue  springs  up  upon  the  sides  of  the  abscess  cavity  and  usually 
soon  fills  it  with  scar  tissue.  (See  Regeneration.)  If  the  cause  con- 
tinues to  act,  as,  for  example,  in  case  of  a  portion  of  dead  and  septic 
bone  beneath  soft  tissue,  a  gangrenous  pulp  in  a  tooth  root  or  infected 
crypts  of  the  abscess  walls,  the  granulation  tissue  breaks  down,  and 
the  condition  is  one  of  ulceration  or  a  chronic  abscess  with  a  fistula. 
If,  in  the  course  of  abscess  formation,  bone  be  encountered  by  the 
pus,  it  may  be  and  often  is  molecularly  broken  down  into  pus.     (See 


IX  FLA  MM  A  TIOX  135 

Acute  Apical  Abscess.)    It  does  not  ahvay>  hajjpen  that  the  pus  finds 

escape  either  naturally  or  through  surgical  aid:  the  patient  may  die 
before  this  occurs,  or  the  tissues  around  the  seat  ot  pus  formation 
may  form  a  boundary  wall  which  the  organisma  fail  to  break  down 
and  thus  die  starved  out.  The  abscess  contents  undergo  changes 
resulting  in  caseation,  or  later  the  mass  may  calcify.  In  tubercular 
caseations  the  tubercle  bacilli  may  live  for  a  long  period.  See  p.  83.) 
The  Streptococci  pyogenes  may  multiply  laterally,  following  the 
subcutaneous  cellular  tissue,  and  produce  violent  spreading  inflam- 
mation with  but  little  pus  formation — e.  g..  some  forms  of  apical 
abscess  and  erysipelas. 

The  products  (toxins;  from  an  abscess  or  infective  inflammation 
may  find  their  way  into  the  blood,  and  a  general  toxemia  result,  or  the 
organisms  themselves  may  enter  the  blood  and  a  general  infection 
result  (septicemia j.  There  are  various  varieties  of  pus  which  have 
names  describing  the  chief  characteristics: 

Creamy  pus  is  the  erroneously  called  laudable  pus  associated  with 
an  acute  abscess  or  ulcer  which  progresses,  as  a  rule,  toward  a  cure. 
It  is  of  a  yellowish-white  color,  creamy  consistency,  and  ^-ithout 
odor. 

Curdy  pus  contains  flakes. 

Ichorous  pus  is  thin,  odorous,  and  irritating. 

Mucopus  is  pus  containing  mucus. 

Seropus  is  pus  containing  much  seriun. 

Sanious  pus  contains  blood. 

Cause. — The  cause  of  suppuration  is  the  development  in  tissues  of 
pyogenic  organisms.  The  action  of  these  causes  is  favored  by  the 
presence  in  the  part  of  a  hj-peremia  or  simple  inflammation,  such  as 
the  injury  introducing  the  organisms  may  cause.  These  as  well  as 
depraved  or  debihtated  tissues  favor  the  action  of  bacteria — i.  e.,  act 
as  predispositions. 

Symptoms. — The  s^Tnptoms  of  suppuration  are  both  general  and 
local. 

Local  Symptoms. — ^The  symptoms  of  inflammation — redness,  heat, 
pain,  and  swelling — occur,  but  usually  much  aggravated.  The  pain  is 
often  of  a  lancinating  character,  sudden  darts  often  following  com- 
parative quiescence.  On  the  other  hand,  the  throbbing  pain  may 
be  continuous  and  intense,  especially  when  the  pus  is  confined  by  bone 
or  tense  tissues,  as  ia  the  case  of  a  felon  or  an  acute  apical  abscess. 
Recalhng  that  around  the  pus  area  there  is  an  area  of  stasis,  next  one 
of  active  but  lesser  inflammation,  and  about  that  hyperemic,  then 
normal  tissue  (Fig.  64),  one  may  judge  of  the  degree  of  involvement 
of  deeper  parts  by  the  appearance  of  the  surface  above  them.    Thus, 


136 


DISTURBANCES  OF   THE    VASCULAR  SYSTEM 


for  example,  hyperemia  at  the  surface  indicates  inflammatory  action 
directly-beneath,  with  a  pus  cavity  still  deeper,  while  inflammation 
at  the  surface,  together  with  hardness  and  tumefaction,  shows  a  more 
involved  condition  of  the  tissue  directly  beneath  it — i.  e.,  a  more 
advanced  state  of  inflammation  or  even  of  suppuration. 

The  softening  of  the  apex  of  the  swelling  gives  a  feeling  of  lessened 
resistance,  indicating  pointing  or  pus  at  the  surface.  In  large,  super- 
ficial abscesses  the  sensation  known  as  fluctuation  may  be  obtained  by 
placing  one  finger  on  one  side  of  the  swelling  and  gently  tapping  upon 
the  other.  Yellowness  of  the  apex,  together  with  softness,  indicates 
that  the  abscess  is  about  to  discharge  its  contents.  A  fistula  or  sinus 
upon  the  surface  is  indicative  of  a  discharged  abscess,  and  leads  to  a 
pus-forming  area  beneath  (chronic  abscess). 

General  Symptoms. — If  toxemia  be  produced  there  may  be  chills, 
and,  at  the  same  time,  fever  as  high  as  104°  F.  A  full,  bounding  pulse 
accompanies  this,  the  patient  is  constipated,  has  a  coated  tongue,  is 
exhausted  by  loss  of  sleep  and  often  disturbed  nutrition  due  to  the 
pain.  There  may  be  other  evidences  of  septic  intoxication,  which 
may  become  profound.    (See  Septic  Intoxication.) 

Leukocytosis  after  surgical  disease  is  considered  pathognomonic 
of  suppuration,  the  count  running  up  to  15,000  or  20,000  per  cubic 
millimeter.     (See  p.  115.) 

Fig.  65 


c  \m(foUdt£(BOQ£ff^oj  ^i^^j^^l^S^^^ 


Tuberculous  ulcer  of  the  intestine:   a,  mucosa;    I,  submucosa;   c,  muscularis;   g,  ulcer; 
t,  tubercle  in  the  mucosa;    t',  focus  caseating  in  the  middle.      X  12. 


Ulceration. — The  development  of  microorganisms  upon  a  free 
surface  causes  tissue  degeneration  and  death,  as  described  under 
Abscess. 

Numerous  forms  of  pathogenic  organisms  are  capable  of  causing 
tissue  degeneration  and  death  of  a  mucous  or  skin  surface.  If  infec- 
tion take  place  through  a  hair  follicle,  or  if  organisms  develop  upon  an 
abrasion,  or  in  the  epithelium  in  conditions  of  general  or  local  debility, 
the  epithelium  is  destroyed  over  an  area,  and  in  the  subepithelial 
tissues  the  organisms  multiply  and  cause  tissue  loss.    If  the  organisms 


INFLAMMATION  137 

he  pyogenic — and  ulcerous  surfaces  are  usually  infected  by  these 
hodies — pus  is  formed  (Fig.  ()5).  Under  some  conditions,  as  in 
debilitated  and  neglected  children,  the  ulcerous  process  may  spread 
rapidly,  as  in  the  cheek  in  cancrum  oris;  or  when  specific  bacilli, 
which  excite  much  swelling  and  quick  death  of  the  tissues  of  the 
cheek,  proliferate,  causing  the  condition  called  noma.     (See  Index.) 

Prognosis. — Abscesses  tend,  as  a  rule,  to  spontaneous  cure  without 
marked  systemic  disturbance.  If  the  pus  discharge  persist  after 
evacuation  of  the  abscess,  persistence  of  the  cause,  or  infection  of  the 
abscess  walls  through  reinfection  or  by  retention  of  bacteria  in  the 
crypts,  is  to  be  suspected.  The  recurrence  of  rigors  (chills)  and  high 
fever  is  a  danger  signal.  A  fluttering,  w^eak  pulse  and  clammy  extrem- 
ities indicate  profound  septic  intoxication,  and  are  indications  for 
local  disinfection  and  systemic  treatment. 

Therapeutics  of  Inflammation. — If  the  cause  of  inflammation  be  in 
evidence  it  must  be  removed ;  good  examples  of  removable  causes  are 
a  splinter  in  the  flesh,  a  gangrenous  tooth  pulp,  etc.  Ordinarily  the 
pus  of  an  abscess  or  an  ulcer  contains  the  cause  (bacteria)  within  it; 
therefore  the  pus  should  be  removed  by  opening  the  abscess,  if  its 
situation  can  be  determined,  after  which  the  pus  cavity  is  syringed  out 
with  germicides,  which  destroy  the  pus  and  the  organisms.  Hydrogen 
dioxid  in  3  per  cent,  aqueous  solution  is  commonly  used;  it  is  made 
more  effective  by  the  addition  of  mercuric  chlorid  (1  to  1000). 

In  ulceration  the  pus  and  organisms  are  destroyed  in  a  similar 
manner,  though  at  times  sloughing  tissue  requires  removal  by  the 
curette,  caustic  agents,  or  by  digesting  agents,  as  caroid,  papoid, 
brewers'  yeast,^  etc. 

Dead  bone  acts  as  a  septic  irritant  and  requires  removal,  and  at 
times  an  abscess  will  remain  persistently  infected,  requiring  surgical 
removal  of  tissue.  The  abscess  or  ulcer,  if  protected  from  further 
infection,  usually  heals  by  formation  of  granulation  tissue.  A  deeply 
seated  abscess  may  require  to  be  packed  with  antiseptic  gauze  (noso- 
phen),  in  order  that  it  may  granulate  from  the  bottom  out;  otherwise 
a  small  orifice  may  heal,  permitting  a  re-collection  of  pus  beneath. 

Ulcers  are  usually  dusted  with  antiseptic  powders,  iodoform,  aristol, 
or  nosophen,  which  cause  drying  of  the  surface  and  prevent  the  access 
or  action  of  organisms.  Under  certain  circumstances  the  presence  of 
suppuration  is  not  certain,  though  phlegmonous  (spreading)  inflam- 
mation is  somewhat  pathognomonic  of  it.  In  such  cases  hot,  moist 
applications,  such  as  hot  poultices,  soften  the  surface  above  the 
abscess  and  determine  its  direction  of  discharge,  thus  limiting  burrow- 

1  Park's  Surgery. 


138  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

ing.  CoLinterirritants  applied  directly  above  the  inflamed  area  also 
hasten  in  snch  cases.  The  stimulation  may  aid  resorption  (destruc- 
tion by  phagocytosis)  of  the  pus  and  resolution  occur.^  The  vascular 
engorgement  in  an  inflamed  part  may  be  reduced  by  local  bloodletting. 

Nancrede  found,  on  dividing  a  vein  upon  the  distal  side  of  an  area 
of  inflammation,  that  after  a  brief  period  the  flow  of  blood  was 
established  through  the  inflamed  area.  Local  bloodletting  by 
leeches  (Gensmer)  produced  even  more  marked  effects.  Drugs  which 
stimulate  the  vasoconstrictors  (ergot),  and  those  which  paralyze  the 
constrictors  (aconite),  lessen  the  blood  pressure  in  the  inflamed  area; 
so  that  if  administered  in  the  early  stages  of  inflammation  they  may 
modify  its  severity.  If,  on  the  contrary,  they  are  administered  after 
stasis  occurs,  they  increase  the  stasis — ergot  actively  and  aconite 
passively.  If  the  flow  of  blood  through  the  inflamed  area  be  reestab- 
lished by  local  bloodletting,  then  the  arterial  sedatives  are  distinctly 
useful  in  lessening  the  flow  of  blood  to  the  part. 

When,  owing  to  vascular  engorgement,  throbbing  pain  is  a  promi- 
nent symptom,  applications  of  cold  are  useful  in  lessening  the  caliber 
of  vessels  and  in  relieving  pain.  But  if  there  be  firm  exudation  and 
marked  stasis,  cold  is  a  detriment.  Heat  then  gives  relief  through 
inducing  a  more  free  flow  of  blood  in  the  collateral  circulation.  Very 
hot  applications  act  as  do  cold  applications,  by  causing  contraction  of 
vessels,  and  may  be  used  to  abort  an  inflammation. 

In  certain  situations,  as  in  case  of  an  inflamed  tooth-pulp,  sedative 
applications,  antiphlogistics,  are  required.  Conjoined  with  local 
measures  of  reducing  vascular  engorgement,  the  use  of  counter- 
irritants  and  general  derivatives  are  indicated,  (See  Treatment  of 
Hyperemia.) 

General  sedatives  are  at  times  demanded  for  the  relief  of  pain. 
Morphin  used  in  small  and  continued  doses  not  only  relieves  pain, 
but  causes  a  contraction  of  small  vessels.  Other  anodynes  are  also 
used  in  this  connection,  as  acetanilid  or  trigemin.  Quinin  and  salol 
are  useful  as  correctives  of  the  intestinal  disturbance,  and  mercuric 
chlorid  in  small  doses  is  useful  as  a  preventive  of  general  infection. 
(See  Acute  Apical  Abscess.) 

REGENERATION  OF  TISSUES. 

Connective  tissues  that  have  been  lost  by  inflammatory  process  or 
operation  are  replaced  by  granulation  tissue  arising  by  mitotic  division 
of  cells  of  the  connective-tissue  group.    The  forms  of  healing  are  by 

^  Park's  Surgery. 


REGENERATION  OF   TISSUES 


139 


first  intention,  second  intention  or  granulation,  healing  under  a  scab, 
and  healing  under  a  clot.     Epithelial  tissues  are  replaced  only  by 


Fig.  66 


Regeneration  of  capillary  bloodvessels:  a,  normal  capillaries;  h,  capillary  process; 
r,  new  capillary  appearing  in  divided  process;  d,  process  undergoing  division;  e,  con- 
necting cell  in  which  no  sign  of  division  has  yet  appeared.    Diagrammatic.    (Green.) 


Fig.  67 


A-  granulating  surface:  a,  layer  of  pus;  b,  granulation  tissue  with  loops  of  blood- 
vessels; c,  commencing  development  of  the  granulation  tissue  into  a  fibriiiated  struc- 
ture.     X  200.     Diagrammatic.      (Rindfleisch.) 


140 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


multiplication  of  epithelial  cells.  The  forms  of  healing  are  practically 
alike  by  formation  of  granulation  tissue,  the  form  being  simply  a 
modification  (of  extent)  of  healing  by  second  intention.  This  granu- 
lative  tissue  is  transformed  into  fibrous  tissue,  the  original  tissue 
rarely  being  reproduced  to  any  great  extent  though  bone  may  be 
regenerated. 

Fig.  68 


Transverse  section  of  granulation  tissue  from  an  open  wound  with  fibropurulent 
deposit:  a,  granulation  tissue;  b,  fibropurulent  deposit;  c,  c,  bloodvessels.  X  150. 
(Ziegler.) 


Healing  by  Second  Intention  or  Granulation. — Shortly  after  evacu- 
ation of  pus  from  an  abscess  the  process  of  repair  is  instituted.  The 
leukocytes  come  to  the  surface  of  the  wound  in  great  numbers;  some 
of  these  may  degenerate  into  pus  cells.  Immediately  beneath  the 
uninjured  connective-tissue  cells  multiply,  forming  embryonic  cells 
(fibroblasts) ;  at  the  same  time  the  endothelial  cells  of  the  capillaries 
multiply  at  points,  throwing  out  solid-pointed  projections  or  buds 


REGENERATION  OF   TISSUES 


141 


from  the  sides  of  the  capillaries  (Fig.  66,  b).  These  lengthen  and 
join  buds  from  other  capillaries  (Fig.  66,  c,  d,  e).  By  mitosis  the 
nuclei  divide  horizontally,  lying  side  by  side  (Fig.  66,  d).  Later  these 
separate  into  two  cells,  discovering  a  lumen  into  which  blood  enters 
from  the  parent  capillary  (Fig.  66,  a',  c).  In  this  manner  loops  are 
formed,  about  which  the  fibroblasts  are  arranged  (Figs.  67  and  68). 

Together  these  form  minute  red  elevations  upon  the  surface  of  the 
abscess  cavity  or  wound,  called  granulations.  Repeated,  the  process 
gradually  fills  the  abscess  cavity. 

Fig.  69 


Laparotomy  wound — sixteenth  day:  «,  a,  epithelium;  6,  6,  corium;  c,  subcutaneous 
fat;  d,  vessels  in  scar  tissue  of  corium;  e,  newly  formed  epithelial  layer;  /,  vessels  in 
subcutaneous  scar  tissue.      X  40.     Modified  from  Ziegler.     (Green.) 


Naturally,  collapse  of  the  walls  or  apposition  of  cut  edges  of  a 
wound  lessens  the  amount  of  granulation  tissue  necessary;  hence,  in 
the  latter  case,  healing  by  first  intention  (with  a  minimum  amount 
of  granulation  or  scar  tissue). 

The  wound  having  been  filled  up,  epithelium  grows  from  the  sides 
and  covers  the  granulations  (Fig.  69,  e).  The  granulation  tissue,  at 
first  highly  vascular,  later  contracts,  and  many  vessels  are  obliter- 
ated so  that  it  becomes  whiter  than  normal  tissue — cicatricial  tissue 
(cicatrix). 


142 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


Fig.  70 


The  indifferent  embryonic  cells  may  have  the  function  of  forming 
any  of  the  connective  tissues.  If  cartilage  is  to  be  formed,  chondrifi- 
cation  takes  place  about  the  specialized  cells.  If  bone  is  to  be  formed, 
certain  cells  form  islets,  about  which  calcification  proceeds.  Nerves 
require  a  month  or  more  to  pierce  the  cicatricial  tissue  (Eichhorst).^ 
In  spite  of  this  assertion  the  writer  finds  that  granulations  are  very 
sensitive  to  touch,  which  seems  clinical  evidence  of  error  in  this 
observation. 

In  healing  beneath  a  scab  the  exudation  and  leukocytes  upon  the 
surface  of  the  wound  dry  into  a  scab  beneath  which  granulations 

and  an  epithelial  covering  are 
formed.  Later  the  scab  falls 
off.  If  prematurely  lost  the 
granulations  are  exposed. 

In  healing  under  a  clot  the 
clot  is  invaded  by  leukocytes, 
which  have  a  solvent  action 
upon  it.  Granulation  tissue 
forms  upon  all  sides  of  it, 
grows  into  it,  and,  at  the  same 
time,  removes  it  by  resorption 
(Fig.  70).  If  the  clot  become 
septic  the  granulations  may  be- 
come infected  and  break  down, 
as  scar  tissue  in  its  early  vas- 
cular stages  is  of  but  feeble 
resistive  power,  though  it  does 
not  absorb  toxins.     (Park.) 

Healing  under  a  clot  is  the 
form  commonly  seen  after 
tooth  extraction.  It  is  an  in- 
teresting point  that  the  alveo- 
lus is  finally  filled  with  bone, 
while  the  original  bony  margins  , 
of  the  alveolus  are  resorbed. 

In  certain  cases  of  abscess 
with  contracted  fistulse  or  open- 
ings of  discharge,  the  orifice  may  close  before  the  granulations  have 
filled  the  pus  cavity.  If  pus  or  an  excess  of  exudate  be  now  formed 
within  the  cavity,  a  second  discharge  may  occur.  To  obviate  this  diffi- 
culty, abscesses  are  often  packed  with  antiseptic  gauze,  so  that  healing 


Absorption  of  blood  clot.  Section  through 
the  margin  of  a  clot  formed  among  the  tissues 
by  extravasation,  showing  the  growth  of 
granulations  by  which  it  is  removed:  a,  a, 
portions  of  clot;  b,  b,  original  tissue;  c,  c, 
granulations  springing  from  the  original  tis- 
sue and  projecting  into  the  clot;  d,  d,  wan- 
dering cells  or  leukocytes  that  seem  to  have 
taken  red  blood  disks  into  their  interior. 
(Section  cut  in  gum  arable  and  stained  with 
hematoxylin.)      X  350.     (Black.) 


Ziegler,  General  Pathology. 


INFLAMMATION  OF  BONE  143 

may  occur  from  the  bottom  of  the  cavity,  while  drainage  is  assured.  In 
other  cases  the  placing  of  a  tent  or  drain  tube  in  the  fistula  together 
with  asepsis  suffice  for  the  attainment  of  the  object.  In  other  cases, 
as  in  bone  cavities,  semisolid  materials,  such  as  Beck's  bone  paste 
are  introduced  to  occupy  the  cavity  to  exclude  infective  and  foreign 
material  while  granulations  form  about  it  and  gradually  absorb  it. 

INFLAMMATION    OF   BONE. 

"Active  inflammatory  changes  may  occur  in  the  periosteum,  the 
medullary  canal,  the  medullary  spaces  of  the  spongy  bone,  and 
the  Haversian  canals,  the  compact  tissue  and  ground  substance 
remaining  passive."^  The  inflammation  is  termed  periostitis,  osteo- 
myelitis, or  osteitis,  the  terms  referring  to  the  point  of  location  of 
the  inflammation — i.  e.,  the  periosteum,  the  medulla,  and  the  spaces 
— the  bone  being  involved  in  all  cases.  Inflammation  of  bone  may 
be  non-infective  or  infective;  the  latter  is  usually  due  to  pyogenic 
organisms — i.  e.,  suppuration  occurs. 

Proliferative  Periostitis. — This  is  a  proliferation  of  cells  of  the 
deeper  layers  of  the  periosteum  combined  with  emigrated  leukocytes. 
A  node  is  thus  formed  which  may  ossify. 

Suppurative  Periostitis.^Pyogenic  organisms  may  enter  an 
injured  periosteum  or  one  weakened  by  previous  disease  {e.  g.,  by 
scarlet  fever).  The  origin  of  the  bacteria  is  by  way  of  the  blood, 
either  directly  or  by  way  of  the  medulla  (as  a  secondary  effect  of 
osteomyelitis),  or  by  way  of  the  skin. 

Pus  forms  beneath  the  periosteum,  raises  it,  and  destroys  its 
connection  with  the  bone.  The  vessels  are  stretched,  damaged,  and 
thrombosis  occurs.  Superficial  necrosis  of  bone  results,  which  may 
be  total  if  other  sources  of  blood  supply  are  also  cut  oft\ 

Acute  Osteomyelitis. — This  is  a  suppuration  occurring  in  the 
bone-marrow,  which  infects  the  bone  proper,  causes  much  throm- 
bosis of  vessels,  coagulation  necrosis  of  bone  cells,  and  may  rapidly 
cause  much  necrosis  of  medullar}^  tissue.  Occurring  in  large  bones, 
much  toxin  is  produced,  which  may  rapidly  cause  death.  The  organ- 
isms and  thrombi  formed,  becoming  emboli,  may  rapidly  lead  to 
pyemia.^    Prompt  surgical  interference  is  called  for. 

Inflammation  of  bone  may  lead  to  its  rarefaction  (rarefying 
osteitis  or  osteoporosis),  its  condensation  (condensing  osteitis  or 
osteosclerosis),  or  its  death  (necrosis  and  caries). 

1  Schmaus  and  Ewiiig,  Pathology  and  Pathological  Anatomy. 
-  Park's  Surgery. 


144 


DISTURBANCES  OF   THE   VASCULAR  SYSTEM 


Fig.  71 


Rarefying  Osteitis  (Osteoporosis). — ^In  the  rarefying  process 
which  occurs  in  chronic  inflammation,  granulation  tissue  is  formed, 
which  enters  the  Haversian  canals  and  spaces  of  spongy  bone  and 

destroys  (resorbs)  the  bone,  owing 
to  the  presence  of  osteoclasts.  They 
thus  form  new  channels  between 
the  spaces — perforating  canal  re- 
sorption (Fig.  71).  With  suppura- 
tion (ulceration)  added,  the  granu- 
lations break  down,  leaving  the 
bone  as  a  dead,  spongy,  or  honey- 
combed mass.  This  is  caries  of  bone. 
In  the  early  stages  the  inflamma- 
tion may  cease,  and  the  bone  not 
only  be  restored,  but  condensed. 
Condensing  Osteitis  (Osteosclerosis). — In  chronic  inflammation, 
of  lesser  degree,  instead  of  rarefaction,  construction  occurs  and  the 
trabeculse  of  bone  may  increase  in  thickness,  so  that  all|spaces  and 


Trabecules   of   bone   with   perforating 
canals.      X  50. 


Fig.  72 


Fig.  73 


Section  of  bone  and  periosteum  cover- 
ing it:  B,  bone;  c,  outer  fibrous  layer; 
a,  inner  layer  of  white  fibrous  tissue;  O, 
layer  of  osteoblasts,  some  of  which  reach 
the  bone  with  their  prolongations.  Nor- 
mal bone.      (Black.) 


Section  of  bone  and  periosteum 
covering  it:  a,  osteoclasts,  cells  that 
absorb  bone;  b,  surface  of  bone, 
showing  fibers  of  periosteum  pene- 
trating it  and  a  Howship  lacuna. 
Lacunar  resorption.      (Black.) 


Haversian  canals  become  smaller.  The  bone  becomes  very  compact 
and  less  vascular,  and  if  built  up  in  excess  of  its  original  dimensions, 
constitutes'the  condition  known  as  exostosis;  if  very  dense,  as  "ivory 


INFLAMMATION  OF  BONE 


145 


Fig.  74 


exostosis."  Both  condensing  and  rarefying  osteitis  occur  about  the 
alveolar  process  and  the  roots  of  teeth.  (See  Hypercementosis 
and  Resorption.) 

Necrosis  of  Bone. — Kecrosis 
of  bone  following  rarefying 
osteitis  is  known  as  caries. 
It  is  a  molecular  death  of 
bone.  Subperiosteal  death  of 
bone  occurs  from  infective 
periostitis,  and  is  due  to  the 
compression  of  vessels  by  the 
exudation  and  to  thrombosis. 
Nutrition  ceases;  death  results. 
The  dead  piece  is  demarked 
by  a  line  of  leukocytes  (phago- 
cytes), solution  of   continuity 

or  rarefying  osteitis  occurs  at  the  line  of  union  with  the  living 
bone,  and   the    piece  is    thrown    out  as  a  sequestrmn.    New  bone 


Lattice-work  figures  in  halisteresis. 
V.  Recklinghausen.) 


(After 


Fig.  76 


Ci  </  ^' 


0." 


i- ■ '''-4-''''  •[} 


i>?  t^^i%s^%^l 


> 


•ft  i„ 


M 


kl 


Diagram  of  healing  frac- 
ture. From  a  guinea-pig 
ten  days  after  injury:  K, 
ends  of  the  bone:  m,  mar- 
row; c,  periosteal  callus; 
d,  medullary  callus;  o. 
osteoid  tissue.      X  0. 


The  same  preparation:  M,  myelogenous  callus; 
P,  periosteal  callus;  K,  ends  of  the  bone;  k,  osteoid 
trabeculge;  o,  osteoblasts  in  rows;  p,  thickened 
periosteum.      X  250.     (Schmaus  and  Ewing.) 


inclosing    a    sequestrum    is    termed    an 
grene.) 
10 


invoJucrvm.       (See    Gan- 


146  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

Resorption  of  Bone. — Under  conditions  of  chronic  inflamma- 
tion bone  is  often  removed  by  neighboring  tissue  in  one  of  several 
ways. 

Lacunar  Resorption. — In  this  form  the  bone  is  excavated  by  giant 
cells  into  bays  called  Howship's  lacunae,  which  may  enlarge,  or  later 
a  reconstructive  action  may  occur  and  osteoblasts  may  fill  up  the 
bays  with  bone.    (See  Hypercementosis  and  Resorption  of  Roots.) 

Perforating  Canal  Resorption, — This  has  been  described  under 
Osteoporosis.  The  canals  connecting  medullary  spaces  are  enlarged 
by  the  granulation  tissue  formed  in  them  (Fig.  71). 

Halisteresis  Ossium. — In  this  form  of  resorption  the  bone  first 
undergoes  decalcification  and  the  matrix  is  later  removed  (Fig.  74). 
It  occurs  in  conditions  of  osteomalacia,  as  in  pregnancy,  senility, 
etc.  It  also  occurs  in  the  alveolar  process,  and  is,  at  least  in  part, 
the  cause  of  the  cleanly  symmetrical  resorption  of  the  gum  and 
alveolar  margins.     (Talbot.^) 

Regeneration  of  Bone. — Bone  lost  by  suppuration  is  first  replaced 
by  provisional  tissue  of  the  connective-tissue  type,  in  which  appear 
osteoblasts.  Calcification  then  proceeds  under  superintendence  of 
these  (Figs.  72,  75,  and  76). 

FEVER. 

The  term  fever  is  applied  to  a  condition  the  most  prominent 
feature  of  which  is  an  elevation  of  the  bodily  temperature  above 
the  normal,  37°  C.  To  constitute  a  fever  this  rise  in  temperature 
must  continue  for  some  length  of  time. 

Etiology. — Fevers  are  commonly  caused  by  the  presence  in  the  circu- 
latory fluids  of  substances  which  act  as  poisons  upon,-  probably,  the 
nerve  centres  controlling  heat  production.  As  a  rule,  the  offending 
substance  is  a  poison  generated  in  the  body  through  the  action  of 
microorganisms.  The  character  and  type  of  the  fever  are  deter- 
mined by  the  nature  of  the  ofi^ending  substances — i.  e.,  the  variety 
of  infection. 

Classes. — Fevers  are  divided  into  periodical  or  continued,  according 
as  to  whether  there  is  a  periodical  fall  of  temperature  and  a  subsequent 
rise,  or  whether  the  fever  continues  practically  unabated  from  the 
beginning  to  the  termination  of  a  disease.  Fevers  are  classed  in 
severity  according  to  the  maximum  temperature,  and,  again,  accord- 
ing to  their  duration.  A  temperature  of  100.5°  to  101.3°  F.  is  called 
slightly  febrile;  101.3°  to  103°  F.,  moderate  fever;  103°  to  105°  F.^ 
marked  fever.    A  temperature  above  106°  F.  is  termed  hyperpyrexia, 

'  Interstitial  Gingivitis. 


FEVER  147 

Symptoms. — The  most  characteristic  symptom  of  fever  is  the  eleva- 
tion of  temperature;  accompanying  this  there  is  an  increased  fre- 
quency of  the  pulse.  In  acute  inflammatory  diseases  the  pulse  is  full 
and  bounding,  the  eyes  injected,  the  bowels  constipated,  and  the 
urine  scanty,  containing  an  excess  of  urea.  On  standing,  the  urine 
throws  down  a  brickdust  deposit  (urates) .  In  fevers  of  a  lower  type, 
or  in  many  fevers  which  begin  as  described,  the  high,  bounding  pulse 
is  succeeded  by  a  soft,  quick  pulse,  and  evidences  of  great  debility. 
In  fevers  in  which  the  temperature  runs  high  there  is  commonly 
evidence  of  intoxication,  more  or  less  delirium,  and  reflex  muscular 
action.  With  a  persistent  temperature  and  a  pulse  becoming  softer 
and  more  frequent,  there  is  increasing  debility. 

Pathology  and  Morbid  Anatomy. — In  all  cases  of  continued  high 
temperature  the  fat  of  the  body  rapidly  disappears  and  granular 
degeneration  occurs  in  the  muscles  and  viscera  of  the  body.  If  the 
fever  be  long  continued  and  of  an  adynamic  type,  this  degeneration 
may  become  marked.  Its  occurrence  in  the  muscles  of  the  heart  is 
common  and  is  an  element  of  danger.  There  are  an  increase  in  the 
amount  of  carbon  dioxid  formed  and  exhaled  from  the  body,  and 
an  increased  amount  of  oxygen  inhaled.  This,  with  the  increase  of 
urea,  the  product  of  the  oxidation  of  nitrogenous  tissues  (muscles, 
glands,  etc.),  indicates  that  the  oxidation  of  the  tissues  is  largely 
increased;  hence  the  elevation  of  temperature.  As  repair  does  not 
equal  waste  in  fevers,  the  nutritive  processes  being  profoundly  dis- 
turbed, the  essential  elements  of  the  tissues  suffer  from  the  increased 
oxidation  and  undergo  degenerative  changes. 

Prognosis. — The  higher  the  temperature  and  the  longer  it  continues, 
the  greater  drain  there  is  upon  the  vital  forces.  As  a  rule,  a  tempera- 
ture of  106°  F.  persisting  more  than  twenty-four  hours  presages 
death.  If  the  vital  forces  flag  and  the  heart  action  becomes  weakened, 
and  if  there  be  evidence  of  profound  intoxication,  such  as  twitching 
of  tendons,  low,  muttering  delirium,  and  a  clammy  surface,  the  out- 
look is  bad.  Favorable  signs  are:  falling  temperature,  a  clear  eye, 
tongue  losing  its  coating,  free  action  of  the  bowels,  free  perspiration, 
free  action  of  the  kidneys,  and  a  good  vascular  tension. 

Treatment. — In  the  light  of  present  knowledge  efforts  should  first 
be  made  to  discover  the  nature  of  the  cause  of  the  fever  and  to  remove 
it,  if  possible.  If  not,  attention  should  be  directed  to  maintaining  the 
vital  forces  until  the  body  rids  itself  of  the  offending  causes.  As 
many  fevers  are  self-limited  in  course  and  duration,  this  latter  treat- 
ment becomes  an  important  consideration.  The  temperature  should 
be  kept  within  safe  limits  by  the  administration  of  antip,yretics, 
when  the  condition  of  the  heart  will  permit  their  use,  and  also  b}^ 


148  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

cool  sponging  or  cool  baths.  The  action  of  the  heart  should  be 
sustained  by  the  administration  of  concentrated  nutriment,  and  by 
stimulants  when  necessary.    The  bowels  must  be  kept  open. 

In  any  form  of  fever  there  is  no  therapeutic  measure  comparable 
with  the  removal  of  the  cause,  provided  this  be  discoverable,  iden- 
tified, and  removable. 

TOXEMIA. 

By  toxemia  is  meant  a  more  or  less  general  disturbance  of  the 
ecomony  as  the  result  of  the  presence  in  the  blood  of  substances 
poisonous  to  a  tissue  or  the  tissues.  The  substance  may  be  a  normal 
constituent  of  the  blood  which  has  accumulated  owing  to  faulty 
elimination — e.  g.,  urea — or  be  derived  from  the  alimentary  canal  as 
the  result  of  unusual  fermentation  therein.  Such  an  effect  is  known 
as  auto-intoxication.  It  may  be  due  to  the  action  of  drugs  of  toxic 
character — e.  g.,  alcohol  or  iodoform.  This  is  drug  toxemia.  Again, 
it  may  be  due  to  the  action  of  the  products  of  bacteria,  which  prod- 
ucts, absorbed  from  certain  foci  of  infection,  produce  general  effects, 
such  as  fever.  Again,  similar  results  can  be  produced  by  the  intro- 
duction of  toxic  products  from  bacterial  culture  in  vitro  or  in  experi- 
mental animals. 

Septic  Intoxication. — By  septic  intoxication  is  meant  the  absorp- 
tion into  the  blood  of  the  products  of  bacterial  activity,  which 
products  are  produced  at  some  focus  or  foci  of  infection  as  the  result 
of  tissue  or  tissue-juice  decomposition.  These  bacterial  products 
produce  symptoms  of  general  poisoning  or  intoxication,  which  are 
mild  or  severe,  according  to  the  character  of  the  poisonous  body 
produced.  The  organisms  do  not  necessarily  enter  the  blood,  hence 
the  blood  is  not  infectious  if  inoculated  into  another  person  (or 
experimental  animal). 

Two  varieties  of  septic  intoxication. may  be  distinguished: 

1.  Intoxication  by  the  products  of  the  action  of  specific  bacteria 
developing  upon  living  tissue. 

2.  Intoxication  by  the  action  of  bacteria  upon  non- vital  materials 
(sapremia) . 

The  action  of  the  bacilli  of  diphtheria,  Asiatic  cholera,  and  tetanus 
are  examples  of  the  first  class.  Their  toxins  are  virulent,  but  the 
bacteria  are  confined  to  the  pharynx,  intestine,  and  the  wound 
respectively. 

Sapremia. — The  entrance  of  putrefactive  or  the  pyogenic  organ- 
isms into  such  material  as  a  large  blood  clot  or  gangrenous  area  may, 
by  putrefaction,  cause  the  formation  of  large  quantities  of  toxins. 
These,  if  absorbed,  produce  rapid  and  profound  symptoms  of  intoxi- 


SEPTICEMIA  149 

cation.  The  symptoms  vary  according  to  the  natnre  of  the  toxin  and 
the  qnantity  absorbed,  bnt  ordinarily  occnr  in  the  following  order: 
Malaise,  rigor,  fever  and  its  symptoms,  nansea,  vomiting,  headache, 
diarrhea,  prostration,  delirium  in  some  cases,  muscular  weakness, 
clammy  skin,  feeble  pulse,  ciuick  respiration,  and  in  fatal  cases  coma 
and  death.  The  symptoms  are  similar  to  those  of  septicemia,  but 
appear  more  rapidly — i.  e.,  septicemia  requires  time  to  spread.  There 
is  a  putrid  wound  which  is  the  source  of  the  toxic  substance.  The 
condition  is  usually  complicated  by  septicemia. 

SEPTICEMIA    (GENERAL   SEPTIC  INFECTION). 

By  septicemia  is  meant  a  condition  in  which  the  bacteria,  usually 
one  of  the  pyogenic  varieties,  gain  entrance  to  the  living  tissues, 
enter  the  circulation,  and  are  carried  to  inaccessible  parts,  where 
their  development  continues  and  from  which  point  their  toxins  are 
absorbed  (Fig.  77). 

This  process  requiring  more  time  than  mere  absorption  of  toxins, 
the  symptoms  are  much  more  delayed  than  in  sapremia.  The  blood 
is  highly  infective  to  susceptible  animals  in  minute  amount,  as  it 
contains  bacteria. 

Pathology. — There  is  a  septic  wound  in  which  incubation  occurs  for 
several  days.  The  lymphatics  leading  from  the  part  and  the  nearest 
lymphatic  glands  become  inflamed.  In  pronounced  cases  the  spleen 
is  enlarged.    There  is  marked  leukocytosis. 

Examination  made  after  death  due  to  the  septic  intoxication 
produced  by  both  sapremia  and  septicemia  exhibits  fairly  constantly 
enlargement  of  the  spleen  and  disintegration  of  the  red  corpuscles, 
with  staining  of  the  intima  of  the  vessels  and  heart.  The  lungs  are 
congested.    Death  occurs  through  heart-failure. ^ 

Symptoms. — These  are  similar  to  those  of  sapremia,  except  that  the 
periods  of  incubation  about  the  body  cause  delays. 

Therapeutics. — For  sapremia  and  septicemia,  the  treatment  is  both 
local  and  general.  The  local  treatment  involves  the  opening  and  dis- 
infection of  all  wounds,  even  the  extirpation  of  a  part  and  of  neighbor- 
ing glands  being  sometimes  necessary  for  removal  of  the  cause.  If 
possible,  the  part  is  immersed  frequently  in  hot  water,  which  may 
occasionally  have  mercuric  chlorid  added  to  it. 

An  antiseptic  salve,  consisting  of  resorcin,  5  parts;  ichthyol,  10 
parts;  unguentum  hydrargyri,  40  parts;  lanolin,  45  parts,  is  to  be 
applied  to  the  area  of  infection.- 

1  Green,  Pathology  and  Morbid  Anatomy.  2  Park's  Surgerj'. 


150  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

Crede's  silver  ointment  may  be  applied  to  the  unbroken  skin  for 
the  systemic  antiseptic  effect  of  the  silver. 

The  general  treatment  consists  in:  (1)  Clearing  the  alimentary 
canal  by  means  of  cathartics  and  maintaining  its  asepsis  by  means 
of  mercuric  chlorid  in  small  doses,  salol,  or  other  suitable  antiseptic. 

(2)  Supporting  the  heart  action  by  means  of  alcohol  and  strychnin, 

(3)  Supporting  the  strength  by  concentrated  liquid  nourishment,  such 
as  egg  albumen,  beef  peptonoids,  beef  juice,  peptonized  milk,^  to 

Fig.  77 

<5    .^  ^ 


1^ 


t, 


/ 


^ 


// 


a 


X    . 


Pectoral  muscle  beset  with  large  numbers  of  the  Streptococcus  pyogenes,  from  a 
case  of  phlegmonous  inflammation  of  the  subcutaneous  and  intermuscular  connective 
tissue,  due  to  cadaveric  poisoning  (the  phlegmon  of  the  wall  of  the  chest  developed 
.  two  days  after  the  finger  was  injured,  and  the  intermediate  lymph  vessels  of  the  arm 
showed  no  evidences  of  being  involved):  a,  perimysium  internum  full  of  streptococci; 
b,  transversely  cut  muscular  fibers,  still  intact;  c,  transversely  cut  muscular  fibers 
which  are  beginning  to  degenerate;  d,  muscular  fibers  into  which  the  cocci  have  pene- 
trated. (Preparation  treated  with  gentian  violet  and  vesuvin,  and  mounted  in  Canada 
balsam.      X  350  diameters.)     (Ziegler.) 


which  diet  fruit  may  be  added. ^  (4)  Reducing  the  temperature  by 
means  of  cold  sponge  baths  or  quinin.  (5)  Maintaining  the  elimina- 
tive  action  of  the  kidneys  until  the  system  has  rid  itself  of  the  toxins. 
For  the  more  profound  cases.  Park  recommends  the  intravenous 
infusion,  as  an  intravascular  germicide,  of  from  500  c.c.  to  1000  c.c. 
of  a  solution  of  Crede's  soluble  silver,  1  to  1000  of  sterilized  water 
at  105°  F.  Streptococcus  antitoxin  is  sometimes  used.  Vaccine 
therapy  is  of  value.    (See  p.  63.) 

1  Thompson,  Practical  Medicine.  ^  Park's  Surgery. 


PYEMIA  151 


PYEMIA. 


By  pyemia  is  meant  a  form  of  septicemia  or  septic  infection  by 
pyogenic  organisms,  which,  locating  at  favorable  spots,  as  in  the 
capillaries,  multiply  and  produce  numerous  abscesses  known  as 
miliary  or  metastatic  abscesses.  From  these  foci  toxins  are  absorbed, 
which  produce  a  septic  intoxication. 

The  organisms  may  enter  the  blood  from  some  focus  of  suppuration 
as  free  cells  or  be  taken  up  by  leukocytes,  or  thrombosis  may  occur  at 
the  original  focus  of  infection,  and  portions  of  clot  be  carried  in  the 
blood  as  septic  emboli  to  terminal  arteries,  where  the  results  of  septic 
infarction  are  set  up.    (See  Infarction.) 

Symptoms. — The  symptoms  of  pyemia  are,  in  general,  those  of 
septicemia;  their  appearance  is  delayed  from  the  date  of  the  reception 
of  an  injury  or  the  outbreak  of  the  primary  suppuration.  The  onset 
of  pyemia  is  usually  by  a  chill  or  a  succession  of  chills.  Each  fresh 
area  of  pus  formation  is  believed  to  be  announced  by  a  chill  and  a 
rise  of  temperature.  The  temperature  is  subject  to  remissions,  and 
sudden  variations  in  its  height  are  noted.  The  general  symptoms  are 
those  of  an  adynamic  fever.  Local  symptoms  appear  according  to 
the  point  of  lodgment  of  septic  emboli.  Pus  centres  may  be  found 
in  the  lungs,  and  cause  symptoms  of  dyspnea;  collections  frequently 
occur  in  joints,  causing  loss  of  mobility;  eruptions  appear  on  the  skin, 
the  swellings  being  apparent;  typhoid  symptoms  become  more  pro- 
nounced, and  an  increasing  debility  ushers  in  a  usually  fatal  ending. 
At  times  both  septicemia  and  pyemia  may  become  chronic. 

Therapeutics. — The  treatment  of  pyemia  should  be  preventive. 
The  carrying  out  of  rigid  antiseptic  precautions  has  much  lessened 
the  frequency  of  pyemia.  If  areas  of  infection  are  removable,  they 
are  removed  no  matter  what  extent  of  operation  may  be  necessary. 
The  general  treatment  is  the  same  as  in  septicemia,  with  much  less 
hope  of  recovery. 

A  consideration  of  the  infective  surgical  processes  in  connection 
with  dental  and  oral  diseases  is  of  the  utmost  moment  to  the  prac- 
titioner of  dentistry.  Nearly  all  of  the  diseases  which  the  dentist  is 
called  upon  to  treat  are  infective  from  their  inception.  Moreover, 
the  saliva,  holding  in  suspension  numerous  forms  of  bacteria,  both 
saprophytic  and  parasitic,  and  their  waste,  is  a  highly  infective  fluid. 

It  has  been  clearly  demonstrated  by  the  researches  of  Miller^  that 
many  forms  of  bacteria  found  in  specific  diseases,  and  found  inhabit- 
ing the  intestinal  tract,  are  more  or  less  constantly  present  in  the 

1  Microorganisms  of  the  Human  Mouth. 


152  DISTURBANCES  OF   THE   VASCULAR  SYSTEM 

liiiiiiaii  mouth,  and  that  the  pathway  in  many  general  infections  is 
no  doubt  via  the  oral  cavity.  A  wound  made  in  the  human  mouth  is 
necessarily  an  infected  wound.  In  the  vast  majority  of  cases  the 
body  exercises  its  protective  function  in  a  phagocytosis/  or  through 
immunizing  processes,  which  disposes  of  invading  bacteria  or  renders 
them  innocuous.  In  other  cases  it  is  beyond  question  that  this 
protective  provision  fails  and  infection  occurs,  especially  if  new  forms 
be  introduced. 

THE   EXANTHEMATA. 

Certain  acute  specific  diseases,  such  as  rubeola,  rotheln,  scarlatina, 
varicella,  and  variola  are  accompanied  by  skin  eruptions  generally 
distributed  over  the  body,  and  which  represent  an  infective  derma- 
titis; indeed,  the  eruptions  of  many  of  these  diseases  are  contagious 
to  other  individuals.  Syphilis,  a  chronic  specific  disease,  due  to  the 
Treponema  pallidum,  produces  similar  effects. 

The  special  interest  lying  in  the  exanthemata  is  that  occurring 
during  the  development  of  the  teeth;  the  latter  are  often  profoundly 
affected,  so  that  malformations,  sometimes  serious  in  character,  occur 
in  the  teeth.  It  is  to  be  recalled  that  teeth  are  dermoid  structures, 
certainly  in  so  far  as  the  enamel  is  concerned.  (See  Malformations 
of  the  Teeth.)  Again,  after  or  during  exanthematous  diseases, 
notably  scarlet  fever,  the  oral  tissues  are  much  debilitated,  so  that 
abscesses  about  the  teeth  may  produce  much  necrotic  tissue  or  the 
disease  itself  may  produce  necrosis. 

1  Hugenschmidt,  Dental  Cosmos,  1896. 


SECTION  II. 

EMBRYOLOGY,  ANATOMY,  AND  HISTOLOGY. 


Fig 


CHAPTER  VI. 

THE  DEVELOPMENT,  ANATOMY,  AND  HISTOLOGY 
OF  THE  JAWS  AND  TEETH. 

As  malformations  of  the  parts  about  the  mouth  and  of  the  teeth 
are  dependent  upon  defective  development  of  the  same,  it  is  incum- 
bent that  certain  facts  concern- 
ing their  embryology  should  be 
stated.  In  like  manner,  as  the 
processes  of  pathology  are  modi- 
fied by  the  peculiar  anatomy  of 
the  teeth  and  associated  parts, 
it  is  necessary  that  a  previous 
knowledge  of  these  be  acquired 
before  the  special  dental  path- 
ology can  be  comprehended. 
The  embryology  of  the  mouth 
begins  at  a  very  early  period — 
before  the  twelfth  day  the  future 
mouth  may  be  located  (His, 
Fig.  78).  The  mouth  and 
nasal  cavity  are  circumscribed 
by  parts  which  are  developed  by 
outgrowths  from  the  head  fold 
of  the  fetus.  Those  structures 
immediately  concerned  are  the 
lateral  tubercles  arising  from 
the    frontal    prominence    (Fig. 


Face  of  an  embryo  of  twenty-five  to 
twenty-eight  days  (magnified  fifteen  times) : 
1,  frontal  prominence;  2,  3,  right  and  left 
olfactory  fossae;  4,  inferior  maxillary  tu- 
bercles, united  in  the  middle  line;  5,  superior 
maxillary  tubercles;  6,  mouth  or  fauces;  7, 
79),  which  grow  downward  and    second  pharyngeal  arch;    8,  third;   9,  fourth; 

forming    the    nose,    the  ^^'  p^'^""*^^"  °°^^^^  ^^^^^^"=   ^^'  p""^^*^"' 


auditory  vesicle.     (Gray.) 


fuse,    tormmg    tne    nose, 

nasal  septum,  the  intermaxillary 

bones,  and  anterior  portion  of  the  upper  lip  (Figs.  80  and  81).    From 

the  sides  of  the  head  fold  at  the  level  of  the  mouth  and  neck  appear 

(153) 


154     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

certain   lateral   protuberances,   or  pharyngeal   arches.        The   first 
pharyngeal  arches  (Fig.  78,  4)  divide  into  (1)  the  superior  maxil- 

FiG.  79 


Sup.  tubercle 
Lateral  tubercle 


Sup.  tubercle 
Lateral  tubercle 


Head  of  an  early  human  embryo,  showing  the  disposition  of  the  facial  fissures  and 
the  superior  and  lateral  tubercles.      (His.) 


S.M.P 


S.M.P. 


-I.M, 


NAS. 


Diagram  illustrating  scheme  of  union  of  the  processes:  N.S.,  lateral  tubercles 
forming  internal  maxillary  bones,  INT.  MAX.,  and  nasal  septum;  S.M.P.,  superior 
maxillary  processes  forming  palatal  processes  of  superior  maxUlse,  S.M.P.;  N.C., 
nasal  cavity;   O.C.,  oral  cavity;   I.M.,  inferior  maxillary  processes  united. 


lary  processes  (Fig.  78,  5)  and  (2)  the  inferior  maxillary  processes 
(Fig.  78,  4,  shown  just  beneath  the  oral  cavity  and  united  in  the 
median  line). 


Fk!.  si 


Complete  bilateral  fissures  (coloboma)  of  face.     (Gucrsant.) 
Fig.  82 


Vertical  transverse  section  through  head  of  human  embryo,  about  the  tenth  week: 
1,  nasal  cartilage;  2,  buccal  cavity;  3,  tongue;  4,  dental  ridge,  lower  jaw;  5,  nasal 
cavity;    6,  dental  ridge,  upper  jaw;    7,  dental  ridge,  lower  jaw.      X  30.     (Broomell.') 


Anatomy  and  Histology  of  the  Mouth  and  Teeth. 


156     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

The  superior  maxillary  processes  develop  the  palate  bones  and  the 
superior  maxillne.  They  form  the  balance  of  the  upper  lip.  The 
arch  itself  forms  the  cheek.  Fig  81,  from  a  case  of  arrested  develop- 
ment, illustrates  the  unions  and  parts  naturally  formed,  but  here 
incomplete.  Fig.  82,  in  which  the  union  of  the  processes  is  still 
incomplete,  shows  how  this  and  cleft  palate  can  occur. 

Secondary  processes  develop  horizontally  toward  each  other,  form 
the  palatal  portions  of  the  superior  maxillae  and  palate  bones,  and 
unite  at  the  median  line  (Fig.  80,  S.M.P.,  also  Fig.  82),  forming  the 
vault  of  the  mouth  and  floor  of  the  nasal  cavity.  Union  occurs  with 
the  lateral  processes,  later  forming  the  intermaxillary  bones  and  bear- 
ing the  germs  of  the  incisor  teeth  (Fig.  83),  thus  completing  the 
formation  of  the  upper  jaw  and  lip. 


Fig.  83 


One  for  nasal  and 
facial  portions. 


One  for  orbital  and  ^^ 
malar  portions,     ua 


Anterior  Surface. 


At  birth. 


One  for  incisive 
portion. 


One  for  palatal 
portion. 


Inferior  Surface. 

Development  of  the  superior  maxillary  bone  by  four  centres,   also  development  of 
intermaxillary  bones.      (Gray.^ 

The  inferior  maxillary  processes  grow  forward  and  unite  at  the 
median  line,  developing  the  inferior  jaw  and  lip.  Fig.  86,  an  arrested 
case,  shows  this. 

The  structures  of  the  floor  of  the  mouth  and  neighboring  structures 
are  formed  from  the  second,  third,  and  fourth  pharyngeal  arches  and 
a  tubercle  arising  near  the  first  pharyngeal  arch.  The  fusions  of  the 
lateral  portions  of  the  upper  maxillae  begin  first  anteriorly  at  about 


Gray's  Anatomy. 


ANATOMY  AND  HISTOLOCIY  OF   THE  JAWS  AND   TEETH     157 


the  eighth  week,  and  progress  posteriorl\'  until  complete  at  about  the 
eleventh.  Malformations  due  to  non-union,  therefore,  date  from 
this  period,  and  consist  of  the  following  typical  varieties: 


Fig.  84 


Fig.  85 


Cleft  of  hard  and  soft  palate;  rudimen- 
tary intermaxillary  bone  placed  in  advance 
of  lips.     (Mason.) 

Fig.  86 


Cleft  of  hard  and  soft  palate. 
(Mason.) 


Median  fissure  of  the  lower  lip  and  chin.      (Marshall,  after  Wofler.) 

1.  Non-union  of  lip  on  one  or  both  sides — simple  hare-lip. 

2.  Non-union  of  lip  and  of  maxilla  and  intermaxillary  bone  on  one 
side  (hare-lip.  Fig.  84). 

3.  Non-union  of  lip  and  intermaxillary  bone  on  both  sides  (double 
hare-lip.  Fig.  SI). 


158     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

4.  Non-union  of  all  horizontal  processes  in  the  median  line  (cleft 
palate,  Figs.  84  and  85). 

5.  Non-union  of  halves  of  soft  palate  (cleft  velum). 

6.  Non-union  of  halves  of  the  uvula  (bifid  or  cleft  uvula). 
Combinations  of  cleft  velum  and  cleft  palate  or  of  cleft  palate  and 

single  or  double  hare-lip  may  exist. 

Figs.  81,  82,  84,  and  88  show  the  parts  in  their  ununited  state. 

The  failure  of  the  inferior  maxillary  processes  to  unite  is  rare, 
but  is  occasionally  seen  (Fig.  86).  The  inferior  maxillary  tubercles 
develop  a  transitory  support  to  the  lower  jaw  known  as  Meckel's 
cartilage.  The  cartilages  of  the  right  and  left  side  do  not  fuse 
together  at  the  future  symphysis.    (Hertwig.)    (See  Figs.  82  and  87.) 


Fig.  87 


Fig. 


M.C. 


Showing  Meckel's  cartilage   (M.C.)   in 
longitudinal  and  transverse  section. 


Osteology  of  hare-lip.     (Museum  of  the 
Philadelphia  Dental  Coellge.) 


It  acts  as  a  support  to  the  fetal  jaw,  undergoes  atrophy  at  about 
the  sixth  month  of  gestation,  and  at  birth  but  few  fragments  are 
found  near  the  symphysis.  At  birth  ossification  has  occurred,  and 
the  bone  consists  of  two  halves  united  by  a  fibrous  symphysis  in 
which  ossification  takes  place  during  the  first  year. 

The  end  of  the  cartilage  in  the  base  of  the  inferior  maxillary  process 
becomes  the  future  malleus  (one  of  the  bones  of  the  middle  ear) .  The 
portion  of  the  cartilage  running  from  the  malleus  to  the  formed  bony 
lower  jaw  becomes  transformed  into  the  internal  lateral  ligament  of 
the  inferior  maxilla.    (Hertwig.) 

A  case  of  failure  of  development  of  the  intermaxillary  bones  has 
been  reported,^  the  space  between  the  cuspid  teeth  being  about 
one-eighth  inch. 


1  Jeffery,  British  Dental  Journal,  July,  1904. 


DEVELOPMENT  OF  THE  TEETH 


159 


It  is  to  be  remembered  that  these  processes  are  formed  by  the  out- 
growth of  the  mesoblastic  layer  of  the  blastoderm,  and  are  covered  by 
epithelial  tissue  springing  from  the  epiblast.  Both  are  concerned  in 
the  formation  of  the  teeth.  Epithelium  is  reflected  over  the  face  and 
oral  cavity.  All  tissues  between  these  layers  of  epithelium  excepting 
the  dental  band  and  enamel  organs  and  the  nerves  are  of  mesoblastic 


origm. 


DEVELOPMENT    OP   THE   TEETH. 


At  about  the  sixth  week  of  gestation,  while  the  maxillary  processes 
are  but  ill-defined  masses  of  mesoblastic  tissue  surrounded  on  all 
sides  by  epiblastic  tissue  (Fig.  89),  the  "dental  hand.'  develops 
as  a  continuous  depression  of 

the  stratum  Malpighii  of  the  ^'^'^-  ^^ 

mucous  membrane  extending 
from  end  to  end  of  the  fetal 
jaw  (Figs.  90,  h,  and  91,  h), 
over  which  depression  is  a 
mound  of  epithelial  cells  de- 
veloped from  it,  and  called 
the  "dental  ridge"  (maxillary 
rampart  of  Kolliker  and  Wal- 
deyer  (Fig.  92,  mr). 

At  ten  points  on  these  bands 
in  each  jaw,  at  about  the 
seventh  to  the   eighth  week, 

a     further     depression     of     the        Porcine    embryo:     ep,    epithelium,    infant 

stratum  Malpighii  occurs,  of  a    ^^^^"^    o?"    stratum    Malpighii;     ct,    embryonal 
°  „    .  connective     tissue     with     large     intercellular 

more  or  less  dehnite  saccular  interspaces.    1.5  cm.    x  250.    (Sudduth.) 
form,  the  sac  also  containing 

embryonic  epithelial  cells  (Figs.  90,  c,  and  92,  3).  This  enlarges  by  an 
interiorward  growth  of  epithelial  cells,  while  the  attachment  to  the 
mucous  membrane  remains  constricted.  x4.t  the  ninth  week  the 
mesoblastic  tissue  beneath  has  somewhat  condensed,  evidencing 
the  first  appearance  of  the  dentinal  papilla.  At  this  stage  the  cord 
(enamel  organ)  has  been  likened  in  appearance  to  a  Florentine  flask 
(Fig.  93,  2).  The  dentinal  papilla  pushes  up  the  base  of  the  enamel 
organ,  which  gradually  adapts  itself  over  the  papilla,  assuming 
first  the  shape  of  a  Phrygian  cap  (Fig.  94),  and  finally  a  saddle  shape 
(Fig.  95).  Just  before  the  connection  of  the  enamel  organ  with  the 
epithelium  of  the  mucous  membrane  is  lost  (as  shown  in  Fig.  95) ;  the 
cord  for  the  corresponding  permanent  tooth  is  given  oft'  from  the  side 
of  the  temporary  cord.    Fig.  95,  cy,  shows  this  after  the  separation. 


160     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 


Fig    91 


At  the  sixteenth  week  the  enamel  organ  has  developed  so  as  to 
contain  three  distinct  formative  parts  concerned  in  enamel  deposition. 

1.  Next  to  the  papilla  the  cells  of  the  stratum  Malpighii  develop 
into  nucleated  columnar  cells,  collectively  defined  by  an  inner  and 
an  outer  limiting  membrane; 
the  ameloblasts,  the  office  of 
which  is  to  deposit  enamel 
(Fig. '97,  e,  and  Fig.  99,  c). 

2.  Those  next  interior  de- 
velop into  large  cells  nutri- 
tivelv     associated     with     the 


Fig.  90 


Vertical  section  through  band 
from  jaw  of  porcine  embryo:  ep, 
epithehum;  h,  band;  c,  cord;  ct, 
connective  tissue.  3.5  cm.  X  00. 
(Sudduth.) 


Longitudinal  transverse  section  of  the 
inferior  maxilla  of  a  porcine  embryo:  b, 
band,  solid  at  anterior  portion,  but  divided 
posteriorly  into  band  and  lamina.  3  cm. 
X  40.     (Sudduth.) 


ameloblasts  and  collectively  called  the  stratum  intermedium  (Fig. 
99,  h);  also  shown  in  Fig.  97  between  b  and  c). 

3.  Those  in  the  central  portion  of  the  enamel  organ  are  large  cells 
rich  in  calcific  material  and  polygonal  from  mutual  pressure,  and 
called  collectively  the  stellate  reticulum.  They  furnish  the  first 
nutritive  material  for  the  enamel  cells  (Fig.  94,  1,  and  Fig.  97,  a). 

The  dentinal  papilla  develops  a  reticulum  of  bloodvessels,  nerves, 
and  branched  stellate  connective-tissue  cells  lying  in  a  gelatinous 
matrix.  Upon  the  surface  of  the  papilla  elongated  nucleated  con- 
nective-tissue cells  called  odontoblasts  are  found,  the  office  of  which 
is  to  deposit  dentin  (Fig.  99,  e;  also  Fig.  122,  Od.).    About  the  enamel 


DEVELOPMENT  OF  THE  TEETH 


161 


organ  and  dentinal  papilla  a  fibrous  sac  develops  from  the  mesoblastic 
tissue,  incloses  them,  and  is  called  the  follicle  wall  (Fig.  95,  c.  ct.), 
and  will  become  the  pericementum  or  cementum  organ.  The  entire 
wall  and  its  inclosures  are  called  the  dental  follicle  (Fig.  95).  At  the 
sixteenth  week  the  cord  of  the  temporary  enamel  organ  gives  off 
from  its  side  a  cord  which  will  form  the  enamel  organ  of  the  suc- 
ceeding permanent  tooth,  and  a  cord  is  given  off  from  the  mucous 
membrane  for  the  first  permanent  molar  (Fig.  95,  cp.).    At  the  seven- 


FiG.  92 


Section  of  jaw,  embryo  of  pig,  showing  growth  of  enamel  organ:  1,  epithelium; 
2,  stratum  Malpighii;  3,  first  stage  in  growth  of  enamel  organ  of  temporary  tooth; 
4,  embryonic  connective  tissue;  5,  developing  bone  of  jaw;  mr,  maxillary  rampart. 
(Andrews.) 


teenth  week  dentin  deposition  begins  by  the  extrusion  of  small 
calcospherites  formed  within  the  odontoblasts,  composed  chemically 
of  calcium  and  magnesium  salts  combined  with  albumin,  a  combina- 
tion known  as  calcoglobulin.  A  cement  substance  is  formed  within 
the  odontoblasts  in  a  manner  similar  to  the  formation  of  inter- 
prismatic  substance  in  the  ameloblast  (Fig.  101).  This  is  extruded 
and  the  calcospherite  pushed  into  it.  An  examination  of  Fig.  123 
shows  this  (as  black  lines).  These  calcospherites  are  evidently  piled 
11 


162     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

into  the  cement  substance  previously  deposited  against  the  amelo- 
blasts,  and  later  against  each  other,  and  around  protoplasmic  pro- 
longations of  some  of  the  odontoblasts,  which  prolongations  remain 
in  similarly  compiled  tube-like  structures  known  as  tubule  walls  or 
sheaths  of  Neuman,  while  the  odontoblasts  themselves  recede,  leaving 
behind  them  a  portion  of  their  substance  in  the  tubules,  and  known 


Fig.  93 


Section  of  jaw,  embryo  of  pig,  showing  growth  of  enamel  organ:    1,  epithelium; 
2,  second  stage  in  growth  of  enamel  organ;  3,  embryonic  connective  tissue.    (Andrews.) 


as  the  dentinal  fibrils.  They  finally  persist  upon  the  surface  of  the 
pulp  (Figs.  99,  100,  110,  122).  Fig.  123,  a  stained  specimen  of  formed 
dentin,  shows  the  arrangement  of  the  compiled  calcospherites.  It 
is  apparently  almost  analogous  to  enamel  formation.  After  some 
dentin  has  been  deposited  enamel  deposition  begins  (at  about  the 
fifth  month) .  The  ameloblasts  in  like  manner  form  within  themselves 
calcospherites   or   enamel   globules,    also   an   amorphous   substance 


DEVELOPMENT  OF  THE  TEETH 


163 


called  interprismatic  cement  substance.  Both  are  calcoglobulin,  and 
yet  contain  less  organic  matter,  at  least  finally,  than  the  dentinal 
calcoglobulin. 

The  ameloblast  first  extrudes  a  drop  of  interprismatic  cement 
substance  against  the  dentin,  and  into  it  deposits  an  enamel  globule. 
(Williams.)  (Fig.  101,  e.)  This  is  repeated,  the  ameloblasts  mean- 
while receding,  the  result  in  finished  enamel  being  a  rod  composed 
of  enamel  globules  united  in  a  row  by  intervening  layers  of  inter- 

FiG.  94 


Section  of  jaw,  embryo  of  pig,  showing  growth  of  enamel  organ  and  dentin  germ: 
1,  enamel  organ;  2,  dentin  germ;  3,  growth  of  jaw;  4,  tongue.     (Andrews.) 


prismatic  cement  substance.  Williams  demonstrates  plasmic  strings 
which  unite  the  various  enamel  globules  to  each  other — probably 
these  give  the  accurate  relation  end  to  end.  The  scheme  of  formation 
is  shown  in  Fig.  101,  and  the  orderly  arrangement  in  Fig.  118.  The 
hexagonal  arrangement  shown  in  transverse  section  (Fig.  119,  B)  is 
due  to  mutual  pressure  of  the  globules.  Each  rod  is  united  laterally 
to  its  neighbor  by  interprismatic  cement  substance,  which  flows 
there  during  deposition  of  each  layer  of  the  enamel.  The  striae  of 
the  enamel  represent  periods  of  incremental  activity.     That  the 


164     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

enamel  rod  is  not  formed  by  calcification  of  the  ameloblast  is  proved 
by  the  fact  that  the  ameloblast  lies  at  an  angle  to  the  developing  rod. 

Fig.  95 


Y 


Veitical  trans\eise  section  of  jaw  of  porcine  embijo  injected  ej  epithelium, 
with  {%l)  infant  layer;  a,  layer  of  ameloblasts ;  o,  layer  of  odontoblasts,  cp,  cord  for 
permanent  tooth;  ot,  outer  tunic;  it,  inner  tunic;  sr,  stellate  reticulum;  wh.  ep, 
whorls  of  epithelium  forced  from  outer  tunic  and  stellate  reticulum;  d,  dentin;  dp, 
dentinal  pulp;  v,  bloodvessels  of  pulp;  ct,  connective  tissue;  c.  ct,  follicular  wall; 
p,  periosteum;    «p,  space.     10  cm.      X  60.     (Sudduth.) 


The  function  of  the  stellate  reticulum  is  to  furnish  calcoglobulin  for 
the  first  enamel  deposition.     This  is  probably  elaborated  in  the 


DEVELOPMENT  OF   TIJE  TEETH 


]  ()5 


stratum  intermedium  and  passed  on  to  the  ameloblasts,  wliicli  con- 
struct the  calcospherites  and  interprismatic  cement  substance.  After 
the  first  deposition  of  enamel  the  stellate  reticulum  disappears  and 
the  papilla-like  structure  of  the  stratum  intermedium  comes  into 
relation  with  the  capillaries  of  the  follicle  wall,  from  which  its  cells 
derive  further  nutrition  and  become  the  originators  of  the  calco- 
globulin  used  in  enamel  deposition  (Fig.  101,  D,  in  which  b  of  Fig. 
97  is  supposed  to  have  disappeared).  After  enamel  completion  the 
ameloblasts  and  remains  of  the  enamel  organ  persist  as  Nasmyth's 
membrane,  a  structure  epithelial  in  character,  ^^^77  in.  in  thickness 

Fig.  96 


Nasmyth's  membrane,  showing  marks  of  hexagonal  ends  of  enamel  prisms. 

by  Barrett.) 


(Section 


(Hopewell-Smith),  and  quite  resistant  to  acids.  Andrews^  describes 
this  as  somewhat  horn-like  and  believes  it  due  to  a  final  merging  of  the 
ameloblasts  and  cells  of  the  stratum  intermedium  with  an  imperfect 
degree  of  calcification.  M.  T.  Barrett  shows  that  its  under  surface 
may  bear  the  hexagonal  impress  of  the  enamel  rods  (Fig.  96).  As 
the  tooth  is  pushed  up  the  enamel  organ  is  carried  with  it,  but  leaves 
behind  it  epithelial  remnants  which  become  included  in  the  follicle 
walls  as  the  epithelial  root  sheath  of  Hertwig  (Fig.  98).  These  are 
claimed  by  Hertwig  to  be  epithelial  remains  or  resting  cells  in  the 
pericementum,  which  have  been  described  by  Black  as  pericemental 
glands.  As  shown  by  Kirk,  these  structures  have  been  previously 
described  by  Hertwig  as  an    epithelial    root    sheath,  the  remains 

1  Dental  Cosmos,  1912,  p.  53. 


166     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

or  trailings  of  the  enamel  organ  left  as  the  tooth  advances  through 
the  area  previously  wholly  occupied  by  the  enamel  organ.  During 
the  development  of  the  follicle,  bone  is  formed  in  islets  which  appear 


Section  of  developing  tooth  of  an  embryo  calf:  a  and  b,  nuclei  of  reticulum  of 
enamel  organ,  showing  spongiose  character;  c,  outer  ameloblastic  membrane;  d, 
inner  ameloblastic  membrane;  e  and  /,  enamel  globules  faintly  showing  nuclear  net- 
work.     X  1000.     (Williams.) 


in  the  mesoblastic  structure  between  the  follicle  wall  and  the  peri- 
osteum (Figs.  92  to  95).  These  gradually  coalesce  until  a  bony  wall 
is  formed  which  constitutes  the  greater  bulk  of  the  fetal  jaw.  The 
cavities  in  the  bone  are  called  crypts,  are  divided  by  septa,  and  are 


DEVELOPMENT  OF  THE  TEETH 


167 


nicely  shown  in  Fig.  104,  which  also  shows  the  relation  of  three  per- 
manent tooth  sacs  to  those  of  their  predecessors.  In  this  figure  the 
outer  plate  of  bone  is  removed,  and  one  is  looking  at  the  outside  of 
the  sac  or  follicle  wall,  of  which  Fig.  102  is  a  transverse  section. 


Fig.  98 


Developing  tooth  showing  Nasmyth's  membrane  over  enamel;   also.  Hertwig's  root 
sheath.     (See  text.)     (Section  by  Addison.) 


Fig.  102  shows  a  dental  follicle  in  an  advanced  stage  of  enamel  and 
dentin  development,  viz.,  at  birth.  Root  form.ation  then  begins,  and 
is  carried  on  by  the  odontoblasts  in  the  papilla  and  cementoblasts  in 
the  follicle  wall  (Fig.  110).  The  odontoblasts  in  the  papilla  form 
dentin,  which  protrudes  beyond  the  dentin  covered  by  enamel. 
In  this  first  formed  dentin  are  spaces  containing  organic  matter,  and 
collectively  known  as  the  granular  layer  of  Tomes  (Fig.  124,  J).  The 
tubules  near  this  are  highly  branched  and  anastomotic.  Coinci- 
dently  with  dentin  formation  the  osteoblasts  in  the  follicle  wall  also 
develop  within  themselves  calcospherites  and  probably  cement  sub- 
stance, which  together  they  deposit  as  cementum  against  the  dentin 
as  a  modified  bone  (subperiosteal  deposition)  and  recede,  leaving 
some  osteoblasts  in  lacunae  (Figs.  105  and  124,  K).  The  finished 
cementum  shows  strata  representing  periods  of  incremental  activity 
(Fig.  124).  It  will  be  noted  that  the  general  mode  of  calcospherite 
and  interspherite  cement  substance  formation  and  deposition  is 
practically  the  same  in  the  ameloblasts,  odontoblasts,  and  osteoblasts ; 


168     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

not  as  to  finished  product,  but  in  principle.  The  foUicle  wall  is 
caught  between  the  developing  cementum  and  bone,  and  persists  as 
a  pericementum,  the  fibers  of  which  attach  them  to  each  other  (Figs. 
102,  C,  and  110,  PER).  Fig.  103  shows  the  various  stages  of  root 
formation,  the  bifurcation  of  roots  being  effected  by  an  upward  pres- 
sure by  the  follicle  wall  against  the  pulp,  in  the  same  manner  as  the 

Fig.  99 


Section  of  developing  tooth  of  an  embryo  calf:  a,  stellate  reticulum  of  enamel 
organ;  b,  stratum  intermedium;  c,  ameloblasts;  d,  dentin;  e,  odontoblasts;  /,  blood- 
vessels— corpuscles  in  situ.     X  275.     (Williams.) 


enamel  organ  is  indented  by  the  papilla.  The  lower  first  permanent 
molar  in  Fig.  115  and  the  third  figure  in  Fig.  103  show  plainly,  by  the 
aid  of  a  little  imagination,  how  this  is  accomplished.  The  dia- 
gram (Fig.  107)  gives  the  ages  at  which  root  calcification  is  complete 
in  the  temporary  set.  The  end  of  the  root  is  composed  entirely  of 
cementum  and  is  therefore  finished  by  the  follicle  wall  (pericemen- 
tum) . 


DEVELOPMENT  OF   THE   TEETH 

Fi(i.   100 


169 


%  OA.i 


^     1  I    '  W    •  ((   ''IP. 


Section  of  growing  tooth  of  calf  at  birth,  showing  fibrils,  fibril  cells,  and  odontoblasts; 
also  the  layer  of  calcoglobulin  and  the  forming  dentin.     (Andrews.) 

Fig.   101 


Mode  of  enamel  deposition:  A,  formed  enamel;  B,  ameloblasts;  C,  secreting 
papillffi  of  stratum  intermedium;  D,  bloodvessels  in  external  fibrous  coat  and  to 
secreting  papillse;  E,  enamel  globules  with  connecting  plasmic  strings;  F,  nuclei 
of  ameloblasts;  G,  blood  supply  of  odontoblastic  layer;  H,  odontoblasts;  I,  im- 
formed  dentin;  /,  formed  dentin.  The  interprismatic  cement  substance  is  shown  as 
smaller  bodies  within  the  ameloblasts.     Semidiagrammatic.     (Williams.) 


170     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 


The  Permanent  Teeth. — These  are  nearly  all  formed  from  cords 
given  off  at  the  sixteenth  week  from  the  sides  of  the  cord  of  the  corre- 
sponding temporary  teeth 
Fig.  102  as  far  back  as  the  bicus- 

-<-K  pids,  which  are  given  off 

from  the  cords  of  the 
first  and  second  tempo-, 
rary  molars  (Fig.  95) ;  the 
sacs  are  formed  and  lie 
lingual  to  and  above  the 
sacs  of  the  temporary 
teeth  (Fig.  113  and  114). 
At  the  fifteenth  week  of 
fetal  life  the  cords  of  the 
first  permanent  molars 
are  given  off  from  the 
mucous  membrane,  at 
the  third  month  after 
birlh  the  cord  for  the 
second  molar  is  given  off 
from  that  of  the  first 
molar,  and  at  three  years 
after  birth  the  cord  of  the 
third  molar  arises  from 
that  of  the  second  molar.  After  eruption  and  root  completion  in  the 
temporary  teeth  and  some  development  of  the  crowns  of  the  perma- 


Developing  tooth  at  birth:  A,  developing  bone; 
B,  tissue  reflected  from  follicular  wall  and  forming 
alveolar  periosteum;  C,  follicular  wall;  D,  vessels 
and  nerves;   E,  epithelium  of  gum. 


Fig.   103 


Pulp  cavities  of  the  superior  first  bicuspid,   from  the  seventh  to  the  twelfth  year. 

(Broomell.i) 

nent  teeth  the  relation  of  the  crypts  of  the  permanent  teeth  to  the 
temporary  teeth  is  as  shown  in  Figs.  112  to  115. 


'  Anatomy  and  Histology  of  the  Mouth  and  Teeth. 


DEVELOPMENT  OF  THE  TEETH 


171 


The  roots  of  the  permanent  teeth  are  developed  during  the  period 
of  the  descent  of  their  crowns  into  the  alveoh  of  the  temporary  teeth, 


Fig.  104 


1,  tooth  sacs  of  deciduous  teeth  turned  out  of  crypts;    2,  lingual  surface  of  mandible. 
The  interior  of  the  crypts  and  septa  shown.      (Broomell.) 

which  occurs  coincidently  with  the  resorption  of  the  temporary  roots, 
which  permits  the  descent.    After  the  shedding  of  the  deciduous  teeth 

Fig.  105 


Transverse  section  through  fused  roots  of  molar  tooth,  showing  interdentinal 
cementum:    1,  interdentinal  cementum.      X  30.      (Broomell.) 


and  the  eruption  of  the  permanent  ones  the  roots  are  completed  after 
variable  periods,  graphically  shown  in  Fig.  116.     Coincidently  with 


172    ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

this  the  jaws  enlarge  in  all  directions  by  resorption  and  new  depo- 
sition of  bone.  Both  the  development  of  the  crowns  and  roots  are 
similar  to  those  occurring  in  the  temporary  teeth. 

Fig.  106 


Persistence  of  Nasmyth's  membrane  in  occlusal  fissure.      (M.  F.  Barrett.) 

The  Histology  of  the  Teeth. — Some  of  the  histology  of  the  teeth 
has  been  given  with  the  description  of  the  development  of  the  teeth, 
and  extended  explanation  is  unnecessary  in  a  work  devoted  to  dental 
pathology.  Some  of  the  structures,  however,  require  some  notice  as 
a  basis  for  pathological  variations,  and  will  be  specially  described. 


Fig.   107 


22  months  after  birth 
18  months  after  birth 

12  months  after  birth 
6  months  after  birth 

40th  week  (birth)  Jli 
30th  week  embryo 
18th  week  embryo 
17th  week  embryo — ^*^ 


Calcification  of  the  deciduous  teeth.     (Peirce.) 

The  Enamel. — The  rods  radiate  as  shown  in  Fig.  117,  but  in  the 
fissures  Nasmyth's  membrane  persists  and  rarely  completes  a  perfect 


DEVELOPMENT  OF  THE  TEETH 


173 


groove,  so  that  a  convenient  location  for  food  and  microorganisms 
remains,  and  dental  caries  is  most  common  at  this  point.  The 
rods  are  wavy  in  outline,  though  sometimes   twisted  or  gnarled. 


Fig.  108 


Injected  tooth,  showing  connection  between  dentinal  tubules  and  lacunae  of 
cementum.     (Von  Beust.) 


Fig.  109 


Injected  tooth,  showing  connection  between  dentinal  tubules  and  enamel  tubes. 

(Von  Beust.) 


They  are  hexagonal  in  cross-section  (Fig.  119).    The  enamel  is  thin  at 
the  cervix,  and  is  usually  overlapped  by  the  cementum,  but  may 


174    ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 


overlap  it,  or  lie  edge  to  edge  with  it  (Choquet).  The  striae  of 
Retzius  are  pigmented  bands,  or  colored  increment.  The  stripes 
of  Schreger  are  cloud-like  markings,  shown  by  Caush  to  be  due  to 
the  presence  of  tubes  in  the  enamel  and  containing  organic  matter. 
Caush  and,  later,  others  have  shown  that  the  enamel  contains 
tubes  into  which  the  dentinal  fibrils  penetrate  (see  Figs.  179,  182, 
and  184).  The  outer  surface  also  may  contain  openings  indicative 
of  present  or  past  organic  contents.     Each  rod  is  composed  of 


Fig.  110 


Fig.  Ill 


Condition  of  third  molar 
at  thirteen  years  of  age. 
(Skiagraphed  by  Custer.) 


Fig.  112 


Diagram  illustrating  root  development  and 
condition  of  an  incomplete  root:  E,  enamel; 
D,  dentin;  P,  pulp  containing  odontoblasts, 
OB;  AP,  alveolar  process;  B,  bone;  C,  cemen- 
tum;  P',  periosteum  of  bone  continuous  with 
the  pericementum;  PER,  pericementum  con- 
taining cementoblasts,  CB;  A,  V,  N,  arteries, 
veins,  and  nerves. 


Showing  the  relation  of  per- 
manent tooth  follicle  to  the 
root  of  the  temporary  tooth. 


enamel  globules  united  end  to  end  by  interprismatic  cement  sub- 
stance, which  also  unites  adjoining  rods  longitudinally  (Fig.  118). 
Von  Beust^  has  shown  by  injecting  pulp  canals  with  a  strong  solution 
of  fuchsin,  also  by  an  arrangement  merely  dipping  the  root  apex  in  the 
above  solution,  that  force  or  even  capillarity  will  carry  the  staining 
fluid  through  the  dentin   into   enamel  and    cementum    (see   Figs. 

Dental  Cosmos,  June,  1912,  p.  660  and  662. 


Fig.  113 


Tooth  follicles  for  deciduous  and  permanent  teeth,  three  months  after  birth:  1,  2, 
tooth  sacs  of  deciduous  teeth;  3,  periosteum  of  hard  palate;  4,  tooth  sacs  of  permanent 
teeth.      (Broomell.) 

Fig.  114 


Deciduous  molars  with  tooth  sacs  for  permanent  bicuspids  attached  to  the  gingival 

tissue.      (Broomell.) 


Fig    115 


View  of  the  upper  jaw  of  a  child,  aged  about  six  and  one-half  years.  The  anterior 
teeth  are  slightly  separated  by  the  partially  developed  permanent  teeth,  lying  behind 
or  posterior  to  them,  pushing  forward  to  occupy  a  more  anterior  position.  The  equal 
height  which  the  crowns  of  the  deciduous  teeth  originally  occupied  is  also  being  dis- 
turbed by  the  advancing  permanent  teeth.     (Feirce.) 


176     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 


107  and  108),  and  shows  conclusively  the  presence  in  enamel  of  canals 
communicating  with  the  dentinal  tubules  and  at  least  permeable  by 
fluids;  also  that  the  dentin  and  cementum  communicate  by  canals. 

The  Dentin.— The  dentin 
is  composed  of  tubules  and 
their  contents  and  intertub- 
ular  substance.  Each  tubule 
contains  a  prolongation  of  an 
odontoblast,  also  called  a 
"fiber  of  Tomes,"  or  denti- 
nal fibril.  The  wall,  differing 
from  intertubular  dentin,  is 
called  the  sheath  of  Neuman 
(Fig.  121). 

The  tubules  are  wavy  in 
direction,  but  radiate  in  the 
crown  and  lie  at  right  angles 
to  the  pulp  in  the  root  den- 
tin. At  the  periphery  the 
tubules  branch  and  anasto- 
mose freely,  and  some  may 
penetrate  the  enamel.  There 
are  also  fine  anastomatic 
connections  at  other  points 
(Fig.  121).  Both  the  tubules 
and  intertubular  substance 
seem  to  be  composed  of  cal- 
cospherites  and  cement  sub- 
stance (Fig.  123). 

The  tubules  are  curved  in 
outline  and  sometimes  show 
a  series  of  short,  sharp 
curves  on  a  general  curved 
level  at  the  points  at  which 
a  new  period  of  increment 
has  occurred.  They  are  the 
stripes  of  Schreger  in  dentin 
or  "incremental  lines"  of 
Salter  (Fig.  190). 

The  Pulp. — This  consists 
of  a  gelatinous  matrix 
in  which  are  imbedded 
branched      connective-tissue 


Fig.  117 


Diagram  of  enamel-rod  directions  and  tubule  curves.    From  a  photograph  of  a  bucco- 
lingual  section  of  a  superior  bicuspid.      (Noyes.) 

Fig.  118 


Section  of  enamel  of  human  tonth.  PliolKgraphed  with  Zeiss  apochromatic  lens 
and  Powel  and  Leiand  apochromatic  condenser.  The  optical  parts  accurately  centred 
and  the  focus  "critical."  The  enamel  rods  are  seen  to  be  resolved  into  distinct  sec- 
tions (enamel  globules),  the  cement  substance  often  passing  entirely  l^etween  the 
sections.  X  400.  (Williams.) 
12 


178     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

cells.  The  odontoblasts  lie  upon  the  surface  next  to  the  dentin, 
with  their  fibrils  extending  into  the  tubules  up  to  the  enamel,  and, 
as  shown  by  Caush,  often  into  it,  forming  organic  matter  in  enamel, 
and  in  some  cases  accounting  for  a  sensitivity  which  is,  however, 
rare. 

Fig.  119 
A 


Enamel  prisms:  A,  fragments  and  single  fibers  of  the  enamel  isolated  by  the  action 
of  hydrochloric  acid;  B,  surface  of  a  small  fragment  of  enamel,  showing  the  hexagonal, 
ends  of  the  fibers.      X  350. 

Fig.  120 


Enamel  showing  both  striation  and  stratification.      X  80  (about).      (Noyes.) 


One  or  more  arteries  enter  the  apical  foramen  or  by  several  fora- 
mina, and  several  veins  may  emerge.    The  arteries  subdivide  in  the 


Fig.  121 


B.C. 


N.Sch. 


Transverse  ground  section  through  the  dentinal  tubules  of  the  first  molar  of  a  child, 
aged  seven  years:  V,  small  connecting  tubule.  Koch's  and  Golgi's  methods  combined. 
X  1200.     (Rose.) 

Fig.  122 


CD.- 


U.D.- 


^T.B. 


P.C. 


•S%' 


-Od. 


^ 


Section  of  pulp,  showing  the  relations  of  the  odontoblasts  to  the  dentin;  Od., 
odontoblasts;  T.F.,  Tomes'  fibers — odontoblastic  processes;  U.D.,  uhcalcified  dentin; 
CO.,  calcified  dentin;   P.C.,  pulp  cells.     X  800.     (Rose  and  Gysi.) 


180    ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

central  portion  of  the  pulp  and  form  a  rich  network  of  capillaries 
beneath  the  odontoblasts. 

The  arteries  are  not  branches  entering  the  foramen  directly  from 
the  bone,  but  rather  branches  of  arteries  in  the  pericementum. 

The  arteries  of  the  pulp  soon  lose  almost  entirely  their  muscular 
coat,  and  their  external  coat  is  reduced  to  an  inconsiderable  amount 
of  fibrous  connective  tissue.  There  is  little  if  any  anastomosis  of  the 
arteries  of  the  pulp,  so  that  collateral  circulation  is  impeded,  though 
not  necessarily  prevented,  as  pathological  cases  show.  The  veins 
remain  for  an  unusual  distance  without  a  muscular  coat,  and  are 
stated  by  Hopewell-Smith  to  be  non-valvular  and  non-collapsible.^ 
These  histological  data  have  great  clinical  significance.  (See  Diseases 
of  the  Pulp.) 

Fig.   123 


Main  mass  of  dentin  of  a  temporary  tooth,  stained  with  chlorid  of  gold,  decalcified 
with  acetic  acid:  F,  F,  dentinal  fibers,  partly  vacuolated;  B,  B,  basic  substance, 
traversed  by  a  reticulum.      X  1200.     (Hart.) 

The  vascularity  of  the  pulp  decreases  with  age.  "  In  young  teeth 
there  are  a  number  of  arterial  trunks  entering  the  apical  foramen, 
which  lessen  in  number  as  the  passage  lessens  in  size."  Finally  only 
one  may  enter.    (Black.) 

The  passage  of  arteries  and  veins  through  a  constricted  foramen 
has  important  consideration  in  connection  with  pulp  diseases.     It 

1  Dental  Cosmos,  1907, 


DEVELOPMENT  OF  THE  TEETH 


181 


has  been  shown  by  Stein^  that  the  arterial  supply  is  through  the 
bone  rather  than  by  direct  arterial  continuity.  (See  Venous  Hyper- 
emia of  the  Pulp.) 

Mummery-  recently  described  the  nerves  of  the  pulp  as  follows: 
The  nerves  enter  by  several  bundles,  and  if  medullated  follow  the 
course  of  the  bloodvessels,  give  off  lateral  branches,  then  lose  the 
medullary  sheath,  near  the  periphery  of  the  pulp,  where  they  break 
up  into  numerous  fine  fibers,  or  axis-cylinders,  and  combine  into 
a  plexus  beneath  the  odontoblasts  (the  plexus  of  Raschow). 


Ground  section  through  the  root  of  a  human  piemolar  D,  dentin;  K,  cement 
corpuscles;  O,  osteoblasts,  Ep,  remains  of  Hertwig's  epithelial  root  sheath  or  peri- 
cemental glands  of  Black ;2    J,  interglobular  spaces.      X  200.     (Rose.) 

From  this  plexus  fine  fibers  pass  between  and  around  the  odonto- 
blasts, which  may  be  inclosed  in  a  fine  netw^ork.  From  these  net- 
works fine  fibers  pass  into  the  tubules  and  continue  to  the  periphery 
of  the  dentin  and  into  the  anastomotic  fibrils. 

The  phenomena  of  sensitive  and  hypersensitive  dentin  shown  an 
evident  physiological  connection.     The  nerves  of  the  pulp  do  not 

'  Items  of  Interest.  2  gee  Dental  Brief,  1912. 

3  The  editor  has  taken  the  liberty  of  altering  the  interpretation. 


182     ANATOMY  AND  HISTOLOGY   OF   THE  JAWS  AND   TEETH 

possess  tactile  sense;  so  their  pains  are  not  localized,  but  reflected, 
as  a  rule.  The  pulp  contains  no  demonstrable  lymphatics,  though 
lymph  spaces  probably  exist;  their  office  is  probably  performed  by 
the  veins,  which  in  other  parts  may  take  up  this  function. '^  The  pulp 
becomes  more  fibrous  and  less  vascular  with  age.  During  health  it 
preserves  the  translucency  of  the  tooth  through  its  relation  with  the 
fibrillse  and  under  certain  circumstances  renews  its  formative  activity 
and  produces  secondary  dentin.  The  forms  of  the  pulps  and  pulp 
cavities  are  shown  in  Figs.  128  to  138. 

Fig.  125 


-N.F 


s.n.J 


X'.G 


Section  of  a  tooth  pulp:  B.V.,  main  bloodvessels  of  pulp;  C,  origin  of  capillaries; 
N.  T.,  m'ain  nerve  trunk;  N.  F.,  subdivisions  of  nerve  into  fibrillse;  Od.,  odontoblastic 
layer;  S.D.,  secondary  dentin;  C.G.,  masses  of  calcoglobulin.  X  30.  (Rose  and 
Gysi.) 

The  Cementum. — The  cementum  is  a  modified  bone  distributed 
over  the  dentin  of  the  root.  It  meets  the  enamel  either  edge  to 
edge,  overlaps  it,  or  is  overlapped  by  it  (Choquet).  In  some  cases 
they  do  not  meet  at  all,  and  leave  the  dentin  exposed.^  It  contains 
lacunae   and   canaliculi,   but  only  rarely  an  Haversian   canal.     It 

1  Green,  Pathology  and  Morbid  Anatomy. 

2  Hopewell-Smith,  Dental  Cosmos,  1909,  p.  1375. 


DEVELOPMENT  OF  THE  TEETH 


183 


contains  a  fibrillar  structure,  which  represents  the  remains  of  vShar- 
pey's  fibers  (Fig.  126). 

The  physiological  function  of  the  cementum  is  to  aflFord  a  means 
of  attachment  of  the  teeth  to  the  maxillary  bones  through  the  medium 
of  the  pericemental  fibers.  In  case  of  death  of  the  pulp,  and,  there- 
fore, of  cessation  of  nutrition  of  the  dentin,  the  vital  relations  of  the 

Fig.   126 


Two 
C. 


fields  of  cementum,  showing  penetrating  fibers:    Gt.,  granular  layer  of  Tomes; 
cementum  not  showing  fibers;  F.,  penetrating  fibers.     X  54  (about).    (Noyes.) 


cementum  and  alveolar  process  are  thus  maintained  and  the  use- 
fulness of  the  tooth  assured.  Whether  the  dentin  can  ever  receive 
nourishment  from  the  cementum  after  pulp  death  has  never  been 
scientifically  shown,  and  the  fact  that  it  may  contain  dead  and  even 
putrefied  material  while  a  healthy  cementum  may  persist,  renders  it 
extremelv  doubtful. 


184     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 


The  Pericementum.  —  {Syn.,  Peridental  Membrane). — The  peri- 
cementum is  the  highly  organized  remains  of  the  folhcle  wall.  As 
the  alveolar  bone  and  cementum  develop  on  either  side  of  it,  it  forms 
also  the  periosteum  lining  the  alveolus.  It  is,  therefore,  the  means  by 
which  the  teeth  are  retained  in  their  sockets  and  a  certain  degree  of 
motion  permitted.  .  The  pericementum  subserves  the  office  of  a 
membranous  attachment  not  altogether  unlike  that  found  in  the 
sutures  of  the  cranial  bones  i 

Fig.   127 


Portion  of  the  side  of  a  root  of  a  tooth,  the  gum  and  alveolodental  membrane,  and 
the  edge  of  the  bone  of  the  alveolus.  A  band  of  fibers  is  seen  passing  over  the  surface 
of  the  alveolus  and  dividing,  some  passing  upward  into  the  gum,  others  passing  more 
directly  across  to  the  cementum.  Numerous  orifices  of  vessels  cut  across  transversely 
are  seen  between  the  tooth  and  the  bone.     (Black.) 

It  is  considered  by  some  observers  that  there  are  two  distinct 
portions  to  the  pericementum,  cemental  and  alveolar.  Photo- 
micrographs generally  do  not  demonstrate  this,  and  it  is  a  matter 
of  difficulty  to  imagine  the  pericemental  bands  divided  into  two 
portions. 

It  is  continuous  with  the  periosteum  on  the  outside  of  the  alveolar 
process,  as  the  sutural  membrane  is  with  the  pericranial  membrane. 

Its  outline  study  divides  the  pericementum  into  three  portions — 
a  gingival,  an  alveolar,  and  an  apical  portion.^ 

'  Noyes,  American  Text-book  of  Operative  Dentistry. 


DEVELOPMENT  OF  THE  TEETH 
Fig.  128 


185 


Transverse  section  of  the  peridental  membrane  in  the  occlusal  third  of  the  alveolar 
portion  (from  sheep):  M,  muscle  fibers;  Per,  periosteum;  Al,  bone  of  the  alveolar 
process;  Pd,  peridental  membrane  fibers;  P,  pulp;  D,  dentin;  Cm,  cementum. 
(Noyes.i) 

1  American  Text-book  of  Operative  Dentistry. 


186     ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND   TEETH 

It  is  composed  largely  of  white  fibrous  tissue  with  interlaced  blood- 
vessels, nerves,  and  glands.  It  also  contains  functional  cells,  fibro- 
blasts, cementoblasts,  osteoblasts,  and  osteoclasts. 


Fig.  129 


Fig.  130 


Fig.  131 


Fig.   132 


Fig.  133 


Fig.  134 


Fig.  135 


Fig.  136 


Longitudinal  and  transverse  sections  of  upper  teeth,  showing  shapes  of  pulp  chambers 

and  their  positions. 


DEVELOPMENT  OF  THE  TEETH 
Fig.   137 


187 


Formalin-gelatin  casts  of  pulp  cavities,  showing  pulp  irregularities.      (Richards.) 

Fig.   138 


Formalin-gelatin  casts  of  pulp  cavities  compared  with  the  teeth  themselves. 

(Richards.) 


188    ANATOMY  AND  HISTOLOGY  OF   THE  JAWS  AND    TEETH 

The  fibrous  tissue  is  made  up  of  principal  fibers  and  indifferent 
fibers.^ 

The  principal  fibers  are  grouped  for  the  most  part  in  bands  or 
bundles  (Fig.  128). 

In  the  alveolar  portion  these  bundles  run  for  the  most  part  from 
the  cementum  to  a  higher  point  on  the  alveolar  process.  The  attach- 
ment is  secured  by  the  penetration  of  the  fibers  into  either  structure. 
This  secures  to  the  tooth,  support  against  direct  pressure  into  the 
socket  and  against  rotary  motion. 

Fig.  139 


Showing  the  buccal  surfaces  of  the  crowns  and  roots  in  position.      (Cryer.) 


At  the  apical  portion  the  bands  have  a  fan-like  distribution.  In 
the  gingival  portion  the  fibers  are  directed  outward  and  slightly 
toward  the  edge  of  the  alveolar  process  for  tooth  support,  or  outward 
and  downward  over  the  edge  of  the  process  to  become  continuous 

1  Noyes,  American  Text-book  of  Operative  Dentistry. 


DEVELOPMENT  OF  THE  TEETH 


189 


with  the  periosteal  fibers,  or  outward  and  upward  with  tlie  sub- 
mucous gingival  tissue,  to  aid  in  the  support  of  the  gum  margin. 
Some  of  the  gingival  fibers  pass  from  the  cementum  of  one  tooth  to 
that  of  the  next  (Fig.  127). 

Kir;.    140 


Vertical  section  of  a  frozen  head,  rear  view.  Shows  relations  of  roots  of  molars  and 
the  maxillary  sinus,  and  of  the  maxillary  sinus  with  the  frontal  sinus.  Wire  passes 
from  the  latter  through  the  infundibulum,  the  hiatus  semilunaris,  and  the  ostium 
maxillare,  into  the  maxillary  sinus,  establishing  a  connection.      (Cryer.) 


190    ANATOMY  AND  HISTOLOGY  OF  THE  JAWS  AND   TEETH 

The  bloodvessels  of  the  pericementum  are  derived  from  several 
sources:  (1)  From  vessels  entering  the  membrane  through  the 
Haversian  canals  of  the  alveolar  process  and  bone,  and  anastomosing 
with  branches  from  the  descending  arteries;  (2)  from  the  vessels  of 
the  outer  periosteum,  coming  over  the  edge  of  the  alveolar  process. 

It  has  been  shown  that  the  destruction  of  main  arteries  as  the 
infra-orbital  or  inferior  dental  does  not  cause  pulp  death,  hence  the 
collateral  blood  supply  is  the  most  important. 

There  are  comparatively  few  capillaries.  The  vessels  lie  mostly 
in  the  outer  or  alveolar  half  of  the  pericementum. 

Fig.  141 


Diagram  of  glands  of  peridental  membrane.      (Black.) 

This  disposition  of  the  arterial  blood  supply  insures  nutrition  to 
the  peridental  membrane  in  case  of  loss  of  the  apical  tissue,  as  in 
case  of  apical  abscess,  and  also  insures  a  collateral  blood  supply 
to  the  pulps  in  case  of  loss  of  main  arterial  trunks,  as,  for  example, 
in  operations  upon  the  inferior  dental  canal,  in  which  case  pulps  do 
not  die.^ 

The  arteries  thus  furnishing  blood  to  the  teeth  are,  for  the  upper 
jaw:  The  anterior  dental  branch  of  the  infra-orbital,  to  the  upper 
anterior  teeth;  the  superior  dental  branch  of  the  alveolar,  to  the  upper 
bicuspids  and  molars  and  the  bone  about  their  root  ends;  the  descend- 
ing palatine  and  its  anastomotic  connection,  the  sphenopalatine, 
supplied  to  the  palatine  side  of  the  upper  alveolar  process,  etc.;  the 
alveolar,  supplied  to  the  buccal  side  of  the  upper  alveolar  process. 

^  John  Bethune  Stein  has  experimentally  proved  this  by  operation  of  removal  of 
the  contents  of  the  inferior  dental  canal.  The  pulps  did  not  die,  and  the  teeth  developed 
as  usual.      Items  of  Interest,  May,  1910. 


DEVELOPMENT  OF  THE  TEETH  191 

In  the  lower  jaw  the  inferior  dental  artery  and  its  incisor  branch 
supply  the  apical  tissues  of  the  lower  teeth  from  the  inferior  dental 
canal.  Its  mylohyoid  branch  supplies  the  gums  and  lingual  perios- 
teum of  the  lower  alveolar  process,  the  mental  branch  supplies  the 
lower  buccal  process  anteriorly,  while  a  branch  of  the  facial  artery 
anastomoses  with  the  mental  anteriorly,  and  the  facial  sends  branches 
to  the  coverings  of  the  buccal  aspect  of  the  lower  jaw  posteriorly. 

Fig.  142 


Glazids  of  Black.     Epithelial  structures:    Ec,  epithelial  cord,  apparently  showing  a 
lumen;  Ch,  cementoblasts;  Cm,  cementum;  D,  dentin.     (See  p.  193  )    (Noyes.) 

With  the  exception  of  those  branches  derived  from  the  facial  artery, 
all  the  blood  comes  from  the  internal  maxillary  artery.  Stein  has 
shown  that  the  blood  is  supplied  to  the  pericementum,  which,  by 
collateral  circulation,  supplies  the  pulp. 

The  veins  return  the  blood  by  similar  channels. 

The  nerves  of  the  pericementum  enter  by  several  trunks  in  the 
apical  tissue,  and  also  enter  from  the  alveolar  wall  and  over  the 
alveolar  edge.  While  their  distribution  is  not  yet  fully  described, 
some  of  them  possess  the  tactile  sense,  as  touch  upon  the  teeth  is 


Fig.  143 


Longitudinal  section:  Eq?,  epithelium  lining  the  gingival  space;  Grj,  gingival  gland 
so-called;  D,  dentin;  N,  Nasmyth's  membrane;  Du,  duct-like  structure  stretching 
away  toward  the  gingivus  from  the  epithelial  cord,  seen  at  Ec\  Cm,  cementum, 
separated  from  the  dentin  by  decalcification.      X  50  (about).     (Noyes.) 


DEVELOPMENT  OF   THE   TEETH  193 

fully  localized.    They  are  derived  from  the  fifth  nerve  and  the  sym- 
pathetic. 

The  Pericemental  Glands. — Black  has  described  gland-like  struc- 
tures lying  in  the  pericementum,  nearer  the  cementum  than  the 
alveolar  wall.  These  are  distributed  over  the  root  in  a  network,  as 
shown  in  Fig.  141. 

They  are  convoluted  cords  of  epithelial  cells  invested  with  a  deli- 
cate basement  membrane,  and  can  be  traced  to  the  epithelium  of  the 
gingival  space,  but  not  to  the  surface. 

Traces  of  a  lumen  have  been  seen,  which,  if  established  as  common, 
would  constitute  them  as  tubes.  Their  function  is  not  definitely 
known,  but  it  is  presumptive  that  they  may  be  secreting  glands  or 
lymphatics.  Some  consider  these  glands  as  resting  epithelial  cells 
derived  from  the  enamel  organ  during  the  upward  movement  of  the 
tooth,  i.  e.,  the  epithelial  root  sheath  of  Hertwig  (Figs.  124,  141, 
and  142).  The  entrance  of  bacteria  from  the  gingival  space  to  deep 
portions  of  the  pericementum,  there  to  develop,  may  possibly  be 
favored  by  their  presence.  They  are  also  considered  as  the  tissue 
in  which  cysts  arise.     (See  p.  165.) 

Glands  of  Serres. — At  the  deepest  portion  of  the  gingival  space 
is  found  a  gland-like  body  which  has  been  given  the  above  name. 
Its  function  is  not  known  (Fig.  143). 

The  Cellular  Elements. — The  fibroblasts  are  spindle-shaped  cells 
destined  to  become  mature  fibers.  They  lie  among  the  other  fibers. 
The  cementoblasts  lie  along  the  cementum  and  are  the  cementum 
builders  (Figs.  72  and  110).  Osteoblasts  are  found  engaged  in 
bone  construction  along  the  alveolar  wall. 

Osteoclasts,  large  multinucleated  cells,  lie  at  points  along  the 
cementum  of  teeth  and  alveolar  bone.  Their  office  is  the  removal  of 
bony  tissue.  They  remove  both  the  organic  and  inorganic  material, 
and  their  eifects  are  seen  upon  the  cementum  and  dentin  of  the 
roots  of  teeth  undergoing  resorption,  also  upon  resorbed  alveolar 
process.  The  excavations  in  which  they  lie  at  work  are  called 
Howship's  lacunae  (Fig.  73). 

Calcospherites  are  sometimes  found  within  the  substance  of  the 
pericemental  membrane,  and  may  have  some  significance  in  relation 
to  its  diseases. 

The  pericementum  in  the  young  is  comparatively  large  and  vas- 
cular, and  in  the  old  becomes  much  attenuated,  more  filjrous,  less 
vascular,  and  subject  to  degeneration. 

Union  of  alveolar  bone  and  cementum  but  rarely  occurs,  though  a 
mechanical  attachment  by  fibrous  pericementum  may  occur.     (See 
Synostosis.)    On  the  other  hand,  the  union  of  the  cementum  of  one 
tooth  with  that  of  another  is  not  uncommon.    (See  Concrescence.) 
13 


CHAPTER  VII. 

DENTITION:  ITS  PROGRESS,  VARIATIONS,   AND 
ATTENDANT  DISORDERS. 

The  process  of  teething,  eruption,  or  dentition  comprises  that 
series  of  vital  operations  which  causes  the  teeth  to  leave  their  crypts 
in  the  maxillae,  to  pierce  the  gum,  and  to  take  their  places  in  the 
dental  arches.  It  is  a  continuation  of  the  process  of  dental  develop- 
ment, and  is  accompanied  and  succeeded  by  root,  alveolar,  and  max- 
illary developments,  which  are  also  to  be  considered  in  connection 
with  it. 

Physiologically,  dentition  is  divided  into  (1)  the  first  dentition,  or 
that  of  the  temporary  teeth,  and  (2)  the  second  dentition,  or  that  of 
the  permanent  teeth. 

Examination  of  Fig.  102  will  show  the  state  of  tooth  development 
at  a  period  shortly  after  birth  (a  central  incisor  being  under  con- 
sideration). The  crypt  is  roofed  over  at  birth  by  a  membranous 
structure.  During  the  period  from  then  to  perhaps  six  months  after 
birth,  about  one-third  of  the  root  will  have  been  formed.  (See  Fig. 
107.)  The  root  end  is  widely  open  (incomplete)  and  the  margins  are 
thin  and  sharp.  A  very  vascular  tissue  occupies  the  space  between 
the  root  and  the  bone,  and  fills  the  interior  of  the  root.  Meanwhile 
the  crown  cusp  will  have  advanced  from  the  situation  shown  in  Fig. 
102  to  a  point  just  beneath  the  mucous  membrane,  which  is  pressed 
up  and  stretched  over  the  advancing  tooth  crown,  presenting  to  oral 
view  a  tumefied  condition  more  or  less  corresponding  to  the  form  of 
the  crown.    This  is  nicely  shown  in  Fig.  144,  A  and  B. 

These  anatomical  data  serve  for  the  consideration  of  the  causes 
and  process  of  eruption. 

Causes  of  Eruption. — It  is  evident  that  there  are  forces  which 
can  bring  about  the  elevation  of  a  tooth  crown  from  its  bed  in  the 
crypt  to  its  position  in  the  mouth. 

The  consideration  of  these  has  led  to  the  development  of  the 
following  rational  theories,  as  well  as  others  now  obsolete : 

1.  That  crown  elevation  is  due  to  the  lengthening  of  the  root — 
i.  e.,  as  root  tissue  is  formed  by  the  pulp  and  follicle  wall  lying  beneath 
and  to  the  side  of  its  edges,  the  tooth  is  mechanically  pushed  up,  the 
tissues  lying  above  it  are  stimulated  and  absorbed,  and  as  more  root 


DENTITION 


195 


Fig.   144 


0 


is  formed,  a  further  extrusion  occurs.  It  is  to  be  noted  that  the  root 
end  occupies  the  same  level,  at  all  stages  of  eruption,  in  the  devel- 
oping jaw  that  was  occupied  by  the  cervical  edge  of  the  crown 
(Fig.  145).  As  no  two  bodies  may  occupy  the  same  space  at  the  same 
time,  the  root-forming  pulp  and  follicle  wall  push  the  tooth  up,  to 
gain  room  for  more  root  formation.  The  mild  continued  pressure  is 
quite  competent  to  do  this.  The  pressure  of  the  soft  tissues  against 
the  root  end  is  explained  by  Constant  to  be  derived  from  the  normal 
blood  pressure.^  That  such  an  internal  pressure  exists  is  shown  by 
the  extrusion  of  ordinarily  confined  parts  when  released  from  the 
accustomed  pressure.  A  simple  accident  demonstrated  this  to  the 
editor.  While  excavating  with 
a  large  bur,  the  softened  dentin 
about  a  decayed  pulp  cham- 
ber, the  cementum  was  widely 
removed  from  the  pericemental 
tissue  beneath,  which  latter 
fortunately  remained  un- 
broken. It  immediately  pro- 
truded into  the  perforation. 
Constant  also  cites  the  extru- 
sion of  a  tooth  in  pericemen- 
titis as  an  evidence  of  the 
influence  of  the  blood  press- 
ure. Another  evidence  is  the 
occasional  rapid  advance  of  a 
tooth  after  lancing  of  the  gum. 

2.  The  process  of  tooth  development  is  a  vital  process,  and  that  of 
eruption  has  been  held  also  to  be.  (Tomes.)  That  cells  concerned 
in  development  seem  to  have  a  predestined  end  or  function  cannot  be 
denied;  at  the  same  time,  throughout  dental  development,  defined 
resistances  to  opposing  forces  seem  to  play  a  part  in  the  moulding  of 
the  soft  and  hard  tissues — e.  g.,  the  depression  of  the  enamel  organ 
by  the  papilla. 

3.  Peirce^  holds  that  the  impact  of  blows  upon  the  jaws  causes  the 
tooth  to  rise  toward  the  gum.  He  explains  the  eruption  of  crowns 
without  roots  upon  this  theory. 

4.  Tomes  explains  the  eruption  of  teeth,  after  development  of  the 
root,  upon  the  theory  that  the  closing  in  of  the  alveolar  process  or 
contraction  of  the  alveolus  upon  the  pericementum  (follicle  wall) 
causes  the  lifting  up  of  the  tooth.    That  such  a  closure  occurs  about 


Lines  of  incision  in  lancing:  A,  A,  over 
the  molars;  B,  B,  over  the  cuspids  and  in- 
cisors before  eruption;  C,  C,  C,  over  the 
molars  and  cuspids  after  partial  eruption. 


1  International  Dental  Journal,  June,  1903. 


2  American  System  of  DentistrJ^ 


196 


DENTITION 


the  extruding  roots  of  teeth  left  after  the  breaking  away  of  the  crowns, 
is  shown  by  examination  of  the  sockets  of  such  roots.  An  abnormaUy 
shallow  alveolus  closed  by  deposition  of  bone  at  its  apex  will  be  found 
in  cases  of  small  apical  portions  of  roots  so  extruded. 

It  is  well  known  that  mild  hyperemia  is  produced  in  pericementi 
which  do  not  receive  a  normal  resistance,  which  would  account  for 
both  the  elevation  and  bone  deposition  on  the  ground  of  blood 
pressure.    (See  Arterial  Hyperemia.) 

Fig.  145 


Diagram   showing   the  upward   movement   of  the   crown   during   eruption   and   root 
development.      (Constant.) 


The  Process  of  Dentition. — Xt  varying  ages,  according  to  the 
state  of  tooth  development,  the  formed  crown  of  the  tooth  advances 
and  presses  upon  the  follicle  wall  overlying  it;  this  is  irritated,  and 
giant  cells  are  developed,  which  by  resorption  remove  this  as  well 
as  the  upper  edge  of  the  wall  of  the  crypt.  The  mucous  membrane 
is  pushed  up  and  moulded  over  the  crown,  thereby  causing  a  tume- 
faction. 

The  mucous  membrane,  at  first  normal  in  color,  becomes  slightly 
hyperemic,  and  then  may  change  to  an  ischemic  condition  and  whiten, 
owing  to  the  removal  of  the  blood  by  the  pressure  of  the  underlying 
crown.  Resorption  from  beneath  causes  a  break  in  the  continuity  of 
the  mucous  membrane,  and  the  crown  tip  erupts  into  the  mouth 
(Fig.  144,  C). 

The  rate  of  resorption  and  crown  advance  are  equalized  in  perfectly 
normal  dentition.     (See  cause  of  pathological  dentition  p.  199.) 

The  crown  rises  from  the  gum,  is  directed  by  the  tongue  and  lip  or 
cheek,  and,  finally,  meets  its  antagonists  of  the  opposite  jaw.  The 
interlocking  of  cusps  and  meeting  of  occlusal  surfaces  limit  further 
movement  of  position. 

Meanwhile  root  development  proceeds,  and  as  it  occurs  the  alveolar 


DEXTTTIOX 


197 


process  is  built  about  the  pericementum,  which  consist  of  the  follicle 
wall  drawn  up.  By  this  means  the  roots  are  firmly  implanted. 
The  further  de\'elopment  of  the  root  proceeds  initil  complete,  and  so 
remains  imtil  iiorlnal  resorption  (if  tlie  temjxjrary  roots  occurs,  and 
for  life  in  the  permanent  teeth. 

The  state  of  formation  of  the  ro(it>  of  temporary  teeth  at  any 
given  age  may  be  judged  l)y  the  table  of  averages  shown  by  Peirce 
in  Fig-.  107.    Being  but  averages,  allowance  for  delays  must  be  made. 

Apart  from  the  presence  of  the  temporary  teeth,  the  process  of 
eruption  is  identical  in  both  sets  of  teeth. 

Periods  of  Eruption. — As  a  general  rule,  the  eruption  of  the 
deciduous  teeth  may  be  said  to  begin  about  the  seventh  month  after 
birth,  and  is  completed  somewhere  about  the  twenty-fifth  month. 
This  rule,  however,  varies  within  wide  limits;  some  children  may  be 
born  with  teeth  erupted;  again,  the  initiation  of  the  process  may  not 
occur  until  the  twelfth  month,  or  even  later. 

The  incisor  teeth  are  usually  ertipted  in  pairs,  the  molars  and 
cuspids  making  their  appearance  in  fotirs.  the  first  molars  in  one 
group,  the  cuspids  in  another,  and  the  second  molars  in  a  third  group. 
The  several  groups  require  different  lengths  of  time  to  complete  their 
eruption,  the  time  occupied  in  the  eruption  of  the  first  molars  being 
longer  than  tltat  required  for  the  eruption  of  the  other  groups. 
Between  the  appearance  of  additional  groups  of  the  teeth  an  interval 
elapses,  no  doubt  a  physiological  provision,  for,  as  will  be  shown 
later,  the  process  of  dentition  is  usually  accompanied  by  evidences  of 
more  or  less  local  disttirbance,  frequently  by  disttirbances  through- 
out the  intestinal  tract,  and  even  reflex  disorders  of  the  central 
ner^'ous  system  occur.  It  is  beUeved,  therefore,  that  the  period 
which  elapses  between  the  eruption  of  the  dental  groups  permits 
the  organism  to  recover  from  the  eft'ects  of  preAdous  disturbance 
before  the  new  source  of  irritation  appears. 

Table.i 


Group  1 

Lower  central  in- 

Time of  eruption, 

Duration  of  eruption. 

Interval 

2  to  3  month.* 

cisors 

7  months 

1  to  10  days 

Group  2 

Upper  central  and 

Time  of  eruption. 

Duration  of  eruption. 

Inter\-al, 

2  months. 

lateral  incisors 

9  months 

4  to  6  weeks 

Group  .3 

Lower  lateral   in- 
cisors 

Time  of  eruption, 
12  months 

Group  4 

First  molars 

Time  of  eruption, 
14  months 

Duration  of  eruption, . 
1       1  to  2  months 

Interval. 

4  to  5  months. 

Group  5 

Cuspids 

Time  of  eruption, 
IS  months 

Duration  of  eruption, 
2  to  3  months 

Interval. 

3  to  5  months. 

Group  6 

Second  molars 

Time  of  eruption, 
26  months 

Duration  of  eruption, 
3  to  5  months 

1  Coleman's  Dental  Surgerj-  (Stellwagen) . 


198  DENTITION 

In  the  above  table  it  will  be  noted  that  the  time  of  eruption  of 
the  lower  lateral  incisors  is  later  than  that  of  the  eruption  of  the  upper 
lateral  incisors.  The  reverse  course  is  frequently  observed;  indeed, 
it  has  usually  been  accepted  as  the  rule  of  precedence  in  the  United 
States.  All  tables,  as  to  periods  of  eruption,  give  but  the  approxi- 
mate times;  while  variations  are  extremely  common.  The  ages 
given  in  this  table  are  those  at  about  which  the  several  teeth  may 
be  expected  to  make  their  appearance.  Stellwagen  (the  American 
editor  of  Coleman),  in  commenting  upon  this  table,  states  that  the 
periods  of  eruption  in  this  country  are  from  one-seventh  or  more, 
earlier  than  the  dates  given.  He  suggests  that  the  difference  in 
food  habit  may  account  for  the  differences  in  time. 

Accompanying  the  development  and  eruption  of  the  teeth,  occur 
developmental  changes  in  all  of  the  glandular  appendages  of  the 
alimentary  canal;  probably  the  alterations  in  their  structure,  and  no 
doubt  in  their  physiological  chemistry,  are  accompanied  by  dental 
provision  for  the  mechanical  subdivision  of  foods  of  postinfantile 
character. 

Symptoms  of  Eruption. — Slight  local  disturbances  are  so  com- 
mon in  even  so-called  normal  first  dentition  as  to  be  accepted  as 
physiological.  The  resorption  of  soft  tissue  around  the  tip  of  the 
crown  of  the  tooth  implies  a  condition  of  mild  non-septic  inflamma- 
tion at  that  point.  In  more  marked  cases  there  is  evidence  of  some 
irritation  cognizable  to  the  infant;  the  gum  is  of  a  somewhat  deeper 
color  and  its  temperature  is  elevated.  Relief  is  afforded  by  pressure, 
which  temporarily  reduces  the  hyperemia,  and  the  child  is  pleased 
to  have  its  gums  rubbed,  to  bite  upon  its  own  or  the  nurse's  fingers, 
upon  rings  or  other  objects.  Still  more  marked  is  the  soothing  effect 
of  biting  upon  cold  substances,  such  as  ice,  which,  in  addition  to 
mechanically  lessening  the  blood  supply,  causes  contraction  of  the 
dilated  vessels. 

Slight  reflex  disturbances  are  evidenced  by  the  stimulation  of  the 
salivary  glands,  which  produces  an  increased  flow  of  saliva. 

Reflex  disturbances  of  more  severe  character  occur  in  pathological 
dentition,  to  be  considered  later. 


PATHOLOGICAL   FIRST   DENTITION. 

The  local  disturbances  may  be  exaggerated  beyond  that  degree 
accepted  as  physiological,  and  may  be  accompanied  by  nervous, 
alimentary,  pulmonary,  or  cutaneous  disturbances.  This  is  patho- 
logical dentition,  and  may  be  of  several  grades  of  severity. 


PATHOLOGICAL  FIRST  DENTITION 


199 


Causes  and  Pathology.— The  primary  cause  of  pathological  dentition 
may  be  stated  as  an  mequality  in  the  rate  of  gum  resorption  and 
crown  advance.  The  advancing  crown  pressing  upon  the  gum  tissue 
causes  irritation;  the  hyperemia  or  mild  aseptic  inflammation  result- 
ing, instead  of  remaining  at  a  point  favoring  the  development  of 
giant  cells  and  resorption,  passes  the  physiological  point  and  causes 
a  disturbance  of  function.  Inflammation,  simple  or  even  infective, 
may  occur  in  the  area. 

Swelling  of  the  gum  occurs,  which,  being  distributed  in  all  direc- 
tions, presses  upon  the  crown,  depressing  it  upon  the  pulp  beneath 
the  sharp  root  margins;  at  the  same  time  the  blood  pressure  of  the 
pulp  tends  to  press  the  tooth  upward.  The  simple  lack  of  resorption 
of  the  gum  would  be  almost  equally  effective  in  preventing  eruption. 
The  sharp  edges  of  the  root  must  irritate  the  sensitive  and  delicate 
pulp  tissue,  which  becomes  inflamed,  and  swollen,  and  still  more 
strongly  urges  the  tooth  upward.  Two  sources  of  disturbance  now 
are  possible:  (1)  the  irritated  gum  tissue  and  (2)  the  irritated  pulp. 
The  latter  is  the  more  likely  to  cause  reflex  disturbances.  Through 
the  intimate  svmpathetic  relations  of  the  fifth  cranial  nerve,  supplied 
to  the  pulp,  with  the  seventh,  ninth,  and  tenth  cranial  nerves  in  and 
about  the  floor  of  the  fourth  ventricle  of  the  brain,  salivary,  muscular, 
nervous,  alimentary,  and  pulmonary  disturbances  become  possible. 

Though  the  pulp  is  more  likely  to  produce  the  reflex  disturbance, 
a  gum  inflammation,  if  intense,  is  often  capable  of  producing  even 
prostrating  svmptoms.  Any  systemic  disturbance— e.  g.,  measles, 
general  debility,  or  lesser  disturbance,  etc.— which  lowers  the  gen- 
eral nutritive  "function  also  in  the  parts  associated  with  the  teeth, 
may  favor  the  production  of  local  pathological  phenomena.  Again, 
systemic  disturbance  readily  produces  a  hyperesthesia  of  the  nervous 
system,  favoring  the  production  of  nervous  phenomena. 

Pathological  dentition  may  occur  in  the  absence  of  an  evident 
hyperemic  gum  tissue.  The  tissue  may  be  white,  showing  ischemia 
from  pressure,  a  binding  down  of  the  root  end  upon  the  pulp  being 
proved  by  the  subsidence  of  symptoms  after  lancing,  and  sometimes 
by  the  rapid,  partial  eruption  of  the  tooth  immediately  after  lancing. 
Again,  pathological  phenomena  have  been  noted  where  no  super- 
ficial local  disturbance  was  evident.  In  these  cases  the  deeper  tissues 
may  exert  a  restraining  influence  upon  the  crown,  but  the  swelling 
is  just  as  probable. 

It  is  to  be  understood  that  the  nervous  and  digestive  systems  ot 
the  child  are  in  a  developmental  condition,  and  therefore  in  unstable 
physiological  equilibrium,  so  that  any  added  physiological  work,  such 
as  unusual  growth  or  dentition,  may  be  more  than  the  organism 


200  DENTITION 

can  endure  without  a  definite  loss  of  general  vital  potential.  This 
may  be  further  complicated  by  hereditary  defects  of  tissue,  such  as 
neurotic,  degenerative,  or  syphilitic  taint,  or  conditions  of  hygiene  or 
feeding  tending  to  lower  the  health  standard. 

Ottofy  offers  the  following  report,  by  the  Bureau  of  Health  of 
Manila,  of  3250  deaths  before  twelve  months  of  age: 

Before  completing  one  month 647 

During  second  and  third  months 302 

Various  causes  not  dental 959 

Four  to  twelve  months  due  to  convulsions  and  eclampsia  .       .       .  1342 

Total 3250 

Showing  a  large  number  of  deaths  due  to  causes  in  which  dentition 
may  have  been  a  determining  or  complicating  factor. 

Dr.  William  P.  Spratley,  medical  superintendent  of  an  institution 
for  epileptics,  states  it  as  his  opinion  that  pathological  first  and  second 
dentition  is  a  determining  cause  of  epilepsy  in  children  having 
neuropathic  taint  in  that  direction.^ 

Symptoms. — The  symptoms  of  pathological  dentition  are  both  local 
and  general. 

Local  Symptoms. — The  local  symptoms  are  usually  those  of  inflam- 
mation, red  and  swollen  gum  tissues  at  times  assuming  a  dusky  hue. 
The  gums  may  be  white,  and  often  glistening,  indicating  their  tense 
stretching  over  the  crowns.  In  the  gum  over  the  erupting  tooth 
there  may  exist  a  vesicular  enlargement  containing  fluid.^  Evidence 
of  local  irritability  is  given  by  the  fact  that  the  child  resists  the 
touching  of  the  gums,  seizes  the  breast  or  bottle  nipple,  and  imme- 
diately releases  it. 

The  readiness  with  which  the  child  will  take  cold  substances,  ice 
or  iced  water,  is  notable  and  self-explainable.  Alternate,  excessive 
flow  of  saliva  and  oral  dryness  are  present. 

In  the  more  marked  cases  of  local  disturbance,  evidences  of  bacterial 
infection  of  the  mucous  membrane  of  the  mouth  may  make  their 
appearance,  such  as  ulcerative  stomatitis.  While,  as  a  rule,  the 
breaking  down  and  ulceration  of  the  tissue  are  confined  to  the  parts 
overlying  the  erupting  teeth,  a  general  stomatitis  or  widely  scattered 
patches  of  ulceration  may  make  their  appearance.  The  localized 
condition  has  been  called  odontitis  infantum. 

General  Symptoms. — The  general  symptoms  may  be  differ- 
entiated into  mild  and  severe. 

The  mild  symptoms  are  such  as  are  attendant  upon  severe  and 
painful  inflammations  about  the  face  at  almost  any  age ;  thus  anorexia, 

1  Dental  Cosmos,  1905.  '■^  Tomes,  System  of  Dental  Surgery. 


PATHOLOGICAL  FIRST  DENTITION  201 

fretfuliiess,  anger,  restlessness,  sleeplessness,  thirst,  mild  fever,  and 
evident  desire  for  the  upright  position  occur.  The  pain  is  at  times 
paroxysmal,  but  may  become  continuous. 

These  symptoms  subside  upon  the  eruption  of  the  tooth  or  lancing, 
though  erupting  cuspids,  bound  by  a  ring  of  tense  gum  tissue  or  by 
adjoining  teeth,  may  continue  the  irritation  even  when  apparently 
erupted  (Fig.  144,  C).  Again,  the  cuspids  may  be  caught  between 
the  lateral  and  first  molar.  The  more  severe  general  symptoms  are 
such  as  are  brought  about  by  reflex  neuroses. 

The  roots  of  the  fifth  cranial  nerves  supplied  to  the  teeth  are  in 
intimate  relation  with  the  roots  of  the  seventh,  ninth,  and  tenth 
cranial  nerves  in  the  floor  of  the  fourth  ventricle,  as  well  as  with 
other  cranial  nerves.  It  may  be  argued  upon  a  priori  grounds  that 
irritation  of  the  peripheral  ends  of  the  fifth  in  the  pulp  tissue  may 
therefore  readily  produce  neurotic  results  in  the  brain,  salivary 
glands,  skin,  lungs,  or  larynx,  intestinal  canal,  or  muscles  of  the  face 
or  extremities. 

Taking  the  intestinal  canal  as  the  most  complicated  example,  we 
find  the  following  data:  The  stomach  and  intestines  are  under  the 
influence  of  the  pneumogastric  nerve,  which  sends  to  its  muscular 
coats  both  stimulant  and  inhibitory  fibers.  Likewise  it  sends  vaso- 
motor fibers  to  the  intestines,  division  of  which  leads  to  inhibition 
of  the  muscular  fibers  of  the  vessels  and  leads  to  vasodilatation 
and  a  great  increase  of  very  watery  succus  entericus.^ 

Intestinal  Disturbances. — That  intestinal  disturbances  may  arise 
independently  of  teething  is  self-evident.  They  are  most  liable 
to  so  occur  during  the  very  period  during  which  teething  may  be 
supposed  to  act  as  a  primary  cause  of  intestinal  troubles;  hence 
differentiation  becomes  important. 

That  the  conditions  may  be  associated  is  also  evident.  As  a  rule, 
intestinal  disturbances  arise  from  improper  feeding,  the  food  acting 
as  an  indigestible  irritant  to  the  stomach  and  intestines.  Even  an 
excessive  quantity  of  good  breast  or  bottle  milk  may,  if  not  regurgi- 
tated, act  as  an  intestinal  irritant.  The  milk  of  an  excited,  exhausted, 
or  debauched  nurse  may  also  act  deleteriously.  Fermentation  due  to 
bacteria  ensues,  and  diarrhea  and  colic  are  a  natural  result. 

Musser^  attributes  these  cases  to  development  of  the  Bacillus  coli 
communis  and  Bacterium  lactis  aeriformis  existing  harmlessly  in  the 
normal  intestine,  but  developing  under  the  abnormal  conditions. 

This  occurring  in  warm  weather,  when  the  child  suffers  from 
intense  heat  has  a  very  debilitating  if  not  fatal  result. 

1  Halliburton,  Kirke's  Physiology,  1896,  p.  684.  2  Medical  Diagnosis. 


202  DENTITION 

The  condition  may  be  viewed  as  an  infective  diarrhea  following 
a  vasomotor  disturbance  of  the  intestinal  walls,  set  up  by  reflexes 
primarily  caused  by  the  indigestible  food.  The  vital  resistance  is 
lowered  by  the  disturbed  alimentation  and  the  pain. 

A  similar  train  of  circumstances  may  be  caused  by  teething. 
Peripheral  irritation  of  terminals  of  the  fifth  nerve  in  the  pulp  may, 
through  the  tenth  nerve,  cause  a  reflex  vasomotor  dilatation  in  the 
walls  of  the  intestines — i.  e.,  hyperemia,  a  condition  which  favors 
bacterial  invasion.  Intestinal  digestion  is  disordered,  the  vital 
resistance  lowered,  and  an  infection  ordinarily  resisted  occurs. 

Diarrhea  may  follow.  In  either  case  alimentation  is  interfered 
with  and  the  general  nutrition  suffers.  The  child  is  debilitated  by 
lack  of  nutrition;  moreover,  toxic  substances  are  generated  in  the 
intestine,  which  cause  a  toxemia,  to  which  many  of  the  general 
symptoms  may  be  attributed,  such  as  fever,  meningitis,  stupor, 
coma,  and  death.  The  general  debility  also  further  interferes  with 
the  process  of  dentition. 

Diagnosis. — A  diarrhea  due  to  improper  feeding  would  not  be 
preceded  by  symptoms  of  pathological  dentition;  would  have  a 
history  of  improper  feeding,  and  possibly  of  unhygienic  conditions, 
such  as  unsterilized  milk  or  milk  bottles,  filthy  surroundings,  etc. 
There  is  a  catarrhal  diarrhea  accompanied  by  vomiting  and  constant 
acid,  watery  stools.  The  stools  may  have  a  chopped-spinach  char- 
acter.   There  is  colic  due  to  collections  of  gas. 

Such  an  infective  diarrhea  may  readily  follow  the  reflex  and 
debilitating  effects  of  pathological  dentition,  as  shown 
above. 

White^  has  noted  that  a  choleraic  diarrhea  may  accompany  and  be 
a  sign  of  pathological  dentition.  Barrett^  states  that  a  diarrhea  due 
to  dentition  will  probably  be  followed  by  constipation. 

A  symptomatic  diarrhea  will,  as  a  rule,  be  accompanied  by  signs 
of  pathological  dentition  at  points  in  the  jaws,  at  which  teeth  should 
be  in  process  of  eruption. 

Nervous  Disturbances.— Disorders  referable  to  the  central 
nervous  system  are  the  most  alarming,  and  are  those  indicating  the 
higher  grades  of  severity  of  irritation. 

The  milder  forms  of  these  are  faint  muscular  twitchings  and 
evidences  of  slight  cerebral  disturbance. 

Either  of  these  may  be  the  result  of  poisons  absorbed  from  the 
alimentary  canal  during  the  course  of  intestinal  fermentation,  but  as 
cases  of  even  convulsions  have  occurred  without  other  cause  than 

1  American  System  of  Dentistry.  2  Qj-al  Pathology  and  Practice. 


PATHOLOGICAL  FIRST  DENTITION  203 

teething  apparent,  and  been  relieved  by  lancing  alone,  the  possibility 
of  direct  connection  between  teething  and  central  nervous  disturbance 
must  be  admitted. 

A  distressing  symptom,  not  easy  to  elicit  on  account  of  the  age  of 
the  patient,  is  headache.  The  child  is  sleepless,  and  cries  without 
apparent  cause;  it  becomes  quiet,  partially  from  exhaustion,  and 
after  a  period  again  commences  sobbing.  The  indication  of  central 
disturbance  may  at  times  be  noted  in  the  contracted  pupils  of  the 
eyes  and  in  throbbing  arteries.  The  usual  treatment,  the  adminis- 
tration of  chloral  hydrate  and  potassium  bromide,  with  cold  appli- 
cations to  the  head,  furnishes  relief  which  is  frequently  not  complete 
without  attention  to  the  dental  organs. 

In  the  more  severe  and  dangerous  cases,  the  evidences  of  disorder 
of  the  central  nervous  system  become  unmistakable.  These  appear 
as  clonic  convulsions  or  symptomatic  eclampsia.  While  it  is  probable 
in  many  cases  that  reflex  irritation  from  the  process  of  dentition  in 
itself  is  but  a  secondary  cause  of  convulsions,  yet  evidence  is  sufficient 
to  warrant  its  being  regarded  as  a  determining  factor.  In  very  many 
cases  teething  convulsions  appear  to  indicate  a  neurotic  family  taint, 
and  eclampsia  may  attend  many  disorders  in  children  of  this  type, 
notably  the  mechanical  and  chemical  irritation  induced  by  the 
presence  of  large  masses  of  indigestible  food  in  the  intestines. 

So-called  teething  convulsions  occur  usually  at  a  time  when  several 
teeth  are  in  process  of  eruption.  The  onset  of  the  convulsion  is 
rarely,  although  apparently  often,  sudden.  If  the  child  be  closely 
observed,  it  is  noted  that  a  period  of  cerebral  disturbance — fretful 
crying,  evidences  of  headache,  sleeplessness,  etc. — is  followed  by  a 
period  of  dulness  and  somnolence,  or  the  child  may  lie  with  eyes 
half  open.  Twitching  of  one  or  more  groups  of  muscles  may  be 
observed;  the  orbicularis  oris  and  other  muscles  of  the  lips,  and  the 
muscles  of  the  eye,  notably  the  superior  and  internal  recti,  ma}^ 
contract  spasmodically.  A  common  muscular  spasm  ushering  in  con- 
vulsions, is  that  of  the  abductor  muscles  of  the  thumb;  the  thumbs 
are  drawn  toward  the  palms  of  the  hands.  The  abductor  muscles  of 
the  feet  contracting,  the  feet  are  drawn  inward.  This  period  may 
be  ushered  in  by  a  sharp  cry,  the  eyes  roll  upward  with  the  lids 
half  open,  and  consciousness  is  lost.  The  symptoms  may  disappear, 
the  child  awakening  dazed  and  fretful;  or  it  may  sink  into  sleep. 
Unless  the  source  of  irritation  be  removed,  or  active  therapeutic 
measures  be  instituted,  the  eclampsia  may  return  and  in  severe 
cases  be  the  precursor  of  death. 

Infantile  paralysis  of  a  group  of  muscles,  or  even  a  single  muscle, 
has  been  recorded,  lasting  from  a  few  days  to  months,  appearing  with 


204  DENTITION 

dentition  and  disappearing  after  it.  In  some  cases  it  persists  for 
life.^    Strabismus,  if  produced,  may  also  persist. 

Skin  Disordeks. — It  is  so  common  as  to  be  almost  termed  the  rule, 
to  find  that  when  there  are  intestinal  symptoms  there  are  eruptions 
observable  on  the  skin.  The  mildest  form  of  these  is  an  herpetic 
eruption  about  the  mouth;  in  other  cases  papular  and  vesicular 
eruptions  are  observed  upon  the  skin  of  the  body  and  limbs. 

Occurring  within  the  mouth,  infection  may  be  added  and  ulcerative 
stomatitis  may  occur  upon  the  gums,  tongue,  lips,  or  inside  of  the 
cheek. 

Pulmonary  Symptoms. — Pulmonary  irritation  may  be  expressed  in 
laryngeal  cough  attending  the  eruption  of  teeth,  and  disappearing 
thereafter. 

Treatment  of  Pathological  First  Dentition. — This  may  be  divided  into 
prophylactic  and  remedial.  The  prophylactic  measures  include  care 
as  to  pasteurization  of  milk  or  modified  milk  diet,  sterilization  of 
bottles,  bottle  nipples  and  rings,  the  prevention  of  the  introduction  of 
unclean  fingers  into  the  mouth  of  the  child,  and  the  antiseptic  care 
of  its  mouth  by  frequent  washings  with  a  saturated  solution  of  boric 
acid  in  water.  This  last  may  be  applied  to  the  mouth  on  a  soft,  linen 
rag  wrapped  on  the  forefinger.  These  measures,  together  with  the 
proper  feeding,  ventilation,  and  care  as  to  clothing,  which  should 
give  comfort  and  not  be  in  any  way  irritating,  tend  to  prevent  intes- 
tinal fermentation  and  to  reduce  the  general  irritability  of  the  infant. 

Remedial  Measures. — To  reduce  local  hyperemia  of  the  gum 
above  an  erupting  tooth,  a  common  domestic  measure  is  valuable,  viz., 
a  small  block  of  ice  is  placed  in  a  corner  of  a  clean  napkin,  and  con- 
fined in  place  by  a  thread ;  the  infant  places  it  in  its  mouth  at  pleasure 
if  old  enough,  or  the  nurse  permits  the  child  to  bite  upon  it.  The 
mechanical  elTect  of  biting  upon  a  hard  substance  has  added  to  it  a 
degree  of  cold  which  lessens  the  local  vascular  engorgement. 

Any  severe  local  irritation  about  erupting  teeth  should  be  relieved 
by  thorough  lancing  of  the  gum.  It  is  irrational  that  the  child  should 
be  permitted  to  suft'er  from  local  irritation  which  may  develop  into 
more  serious  complications. 

This  operation  is  performed  by  dividing  the  gum  lineally  over  the 
incisors  and  cuspids  before  eruption,  crucially  over  the  cuspids  after 
eruption  of  the  cusps  only,  crucially  over  the  upper  first  molar,  and 
with  an  X-incisor  over  the  upper  second  and  lower  first  and  second 
molars  (Fig.  144). 

For  severe  cases  Flagg  advised   the  removal  of  a  block  of  gum 

1  White,  American  System  of  Dentistry. 


PATHOLOGICAL  FIRST  DENTITION  205 

from  over  a  molar.  A  cut  is  made  parallel  with  the  lingual  side  of 
the  crown,  a  second  parallel  with  the  buccal  side,  a  third  parallel 
with  the  mesial  side.  A  tenaculum  is  thrust  into  the  block  of  gum, 
which  is  drawn  tense,  and  then  divided  at  the  distal  portion,  prefer- 
ably with  a  pair  of  curved  gum  scissors.  Lacking  these  latter,  the 
bistoury  may  be  used. 

The  cut  over  the  upper  incisors  should,  if  possible,  be  made  a 
little  to  the  outside  of  the  cutting  edge,  that  for  the  lower  to  the 
inside,  in  order  that  their  crowns  may  take  a  proper  direction  toward 
occlusion. 

The  instrument  to  be  used  is  a  sharp-pointed  bistoury,  as  it 
penetrates  well  and  permits  a  free  draw  cut.  It  is  to  be  wrapped 
with  tape  or  a  strip  of  linen  cloth  until  only  one-quarter  of  an  inch  of 
the  point  is  exposed.  This  precaution  prevents  accidental  wounds. 
The  child  must  be  securely  held  by  an  assistant,  the  least  sympathetic 
available. 

Flagg's  method  was  to  place  the  child  upon  its  back  across  the 
lap  of  the  assistant,  who,  in  one  position,  places  his  left  hand  over  the 
child's  eyes,  securing  the  head;  his  right  hand  secures  the  hands  upon 
the  abdomen,  while  the  legs  are  held  against  his  body  by  the  right 
arm.  The  position  may  be  exactly  reversed.  The  feet  should  be 
placed  toward  the  light  for  the  upper  jaw,  the  reverse  for  the  lower 
jaw.  In  another  position  the  child  sits  upon  one  thigh  of  the  assist- 
ant, the  back  of  the  head  resting  upon  the  chest,  and  the  hand  of  that 
side  (usually  the  right)  pressed  upon  the  child's  forehead  to  hold  the 
head  firmly.  The  other  hand  and  forearm  hold  the  child's  hands 
and  legs  firmly. 

The  operator  encloses  the  gum  about  the  part  to  be  cut  with  the 
thumb  and  forefinger  of  the  left  hand,  so  that  the  bistoury  cannot 
slip  and  cut  lip,  cheek,  or  tongue.  Incision  over  the  erupting  tooth 
should  be  made  until  the  knife-blade  is  felt  to  touch  the  enamel 
surface.  The  operation  of  scarifying  the  gums,  making  merely  a  few 
scratches  to  relieve  engorged  vessels,  is  but  temporizing  with  the 
condition;  the  cut  should  be  of  sufficient  extent  to  entirely  remove 
tension  from  above  the  tooth.  The  little  finger  of  the  right  hand  may 
rest  upon  the  chin  of  the  child  as  an  additional  guard. 

If  the  child  bite,  a  cork  with  a  string  attached  for  safety  may  be 
used  as  a  prop. 

More  or  less  bleeeding  follows  upon  the  operation,  and,  as  a  rule, 
ceases  spontaneously.  A  short  period  of  bleeding  is  desirable,  so  that 
vascular  engorgement  may  be  reduced.  Suckling  by  the  breast  or 
bottle  usually  serves  to  check  the  bleeding;  the  tissues  about  the  cut 
surfaces  are  compressed  by  tongue  and  lips  during  suckling,  and 


206  DENTITION 

bleeding  ceases.  In  the  event  of  the  bleeding  continuing,  the  mouth 
should  be  carefully  examined,  and  a  piece  of  ice  in  a  napkin  may  be 
given  to  the  child  to  suck.  The  child  may  swallow  the  blood  and  later 
regurgitate  it.  Obstinate  bleeding  may  require  the  use  of  styptics, 
but  these  should  be  of  a  character  to  cause  only  coagulation  of  the 
blood,  not  the  destruction  of  tissue.  A  little  powdered  tannin  laid 
upon  the  cut  acts  promptly,  as  does  also  a  small  amount  of  powdered 
alum.  In  some  cases  the  internal  treatment  may  be  necessary. 
(See  Hemophilia.) 

Death  has  occurred  from  hemorrhage  due  to  lancing,  in  cases  of 
presumably  hemorrhagic  diathesis;  so  that  inquiry  as  to  family 
history  would  be  a  wise  precaution.  Obtaining  such  a  history,  the 
gravity  of  the  symptoms  alone  warrant  the  operation.  In  the  absence 
of  such  a  history  the  operation  is  to  be  held  as  trivial.  If  it  occurs,  it 
should  be  treated  as  indicated.     (See  Hemophilia.) 

The  operation  of  lancing  is  warranted,  even  when  the  gum  may 
be  likely  to  heal  over  the  tooth  by  formation  of  cicatricial  tissue,- 
provided  symptoms  demand  it.  It  is  contra-indicated  in  diphtheria 
and  erysipelas,  owing  to  the  danger  of  infection. 

Shock  has  occurred  in  long-continued  debilitated  cases,  and  if 
feared,  a  trifle  of  brandy  in  water  may  be  given  previous  to  the 
operation. 

It  is  within  the  knowledge  of  the  writer,  that  a  physician  has  refused 
to  lance  the  gums  in  a  case  diagnosticated  as  cerebral  meningitis, 
even  when  death  was  prognosticated  and  though  the  child  was  at 
an  age  rendering  pathological  dentition  possible,  and  in  spite  of  a 
history  of  pathological  dentition  in  a  previous  child  at  the  same  age. 
J.  Lewis  Smith^  concedes  the  similarity  of  occasional  symptoms  of 
pathological  dentition  and  cerebral  meningitis,  so  that  the  above 
therapy  was  foolish,  to  say  the  least,  and  especially  so  in  view  of  the 
probable  death,  which  did  occur.  In  many  desperate  cases,  lancing 
has  effected  marvelously  rapid  recoveries,  aided  by  judicious  handling 
of  the  accessory  symptoms,  even  though  all  hope  from  ordinary 
therapy  had  been  abandoned. 

Treatment  of  Stomatitis. — Should  general  stomatitis,  with  or 
without  stomatitis  ulcerosa,  make  its  appearance,  the  mouth  is  to  be 
promptly  and  freely  sprayed  with  a  3  per  cent,  solution  of  hydrogen 
dioxid,  followed  by  a  spray  of  potassic  chlorate  (gr.  xx  to  §j),  which 
usually  affords  prompt  relief.  Should  the  spots  of  ulceration  not 
disappear  promptly,  the  mouth  and  tissues  about  the  ulcer  are  to 
be  guarded  by  soft  linen  napkins;  each  ulcer  is  dried  and  touched 

1  Diseases  of  Children. 


PATHOLOGICAL  FIRST  DENTITION  207 

with  carbolic  acid,  full  strength.     The  spraying  is  to  be  repeated 
at  intervals  of  three  hours  during  the  waking  period. 

Treatment  of  Skin  Eruptions.— The  eruptions  which  appear 
upon  the  skin  during  dentition  may  be  a  source  of  annoyance  to 
the  child  by  causing  itching.  As  a  rule,  measures  directed  toward 
a  regulation  of  the  intestinal  functions  cause  a  disappearance  of  the 
skin  affections.  If  the  eruption  be  widespread  and  cause  much 
itching,  a  wash  of  phenol-sodique,  diluted  to  one-third  with  water, 
usually  affords  relief.  If  the  surfaces  be  then  dried  and  talc  powder 
dusted  over  them  the  condition  is  much  alleviated.  About  the  mouth 
and  over  excoriated  surfaces  a  zinc  oxid  ointment  is  useful. 

Treatment  op  Intestinal  Symptoms. — The  fermentative  material 
in  the  bowel,  together  with  the  great  mass  of  bacteria  present,  should 
be  removed  by  the  use  of  a  cathartic.  It  is  indicated  in  both  con- 
stipation and  diarrhea.  Castor  oil  serves  well,  and  is  readily  taken 
by  children.  To  lessen  the  irritation  of  the  bowel,  laudanum  and 
powdered  acacia  may  be  added. 

The  following  formula  may  safely  be  used  even  at  six  months  of 
age: 

I^ — Tincturse  opii gtt.  x 

Olei  ricini    . 151SS 

Pulveris  acacise '     •      ■      ■     oLl 

Saccharini ^^'..V 

Aquae  cinnamomi q.  s.  ad    fgii.!      M. 

Sig.— Shake  the  bottle,  and  give  one  teaspoonful  each  two  hours  if  needed. 

For  an  additional  six  months  of  age,  ten  drops  more  of  laudanum 
may  be  added  to  the  general  formula.  In  mild  cases,  olive  oil  in  half- 
teaspoonful  doses  may  be  substituted. 

Following  catharsis,  antacid  sedative  astringents  and  intestinal 
antiseptics  are  indicated: 

I^— SaloH 3.i. 

Bismuthi  subnitratis OU 

Misturse  creta; ad  fgiij — M. 

Sig. — One  teaspoonful  every  four  hours.      (Biddle.) 

I^— Tinctura3  opii gtt.  xvj 

Bismuthi  subnitratis 3ij 

Misturse  cretse foiss 

Syr.  simp fgiss— M. 

Sig. — Shake  well,  and  give  in  teaspoonful  doses  every  four  hours.      (Barrett.) 

The  virtues  of  both  formula;  may  be  obtained  by  including  the 
laudanum  (gtt.  xii)  with  the  salol  formula. 

Listerine  in  10-drop  doses,  in  water,  every  three  hours,  serves 
as  an  intestinal  antiseptic. 


208 


DENTITION 


The  gums  are,  of  course,  to  be  lanced  at  the  outset,  if  the  diarrhea 
be  due  to  pathological  dentition.  Following  the  intestinal  antisepsis, 
the  general  debility  and  possible  intestinal  toxemia  (see  p.  207)  are 
to  have  careful  attention,  and  the  child's  food  is  to  be  properly 
adjusted  to  its  needs. 

J.  Lewis  Smith  claims  that  upon  the  following  diet,  ill-conditioned 
children  under  his  care  in  the  hospital  escape  summer  diarrhea  and 
thrive;  the  diet  is  therefore  here  introduced. 

For  children  not  nourished  on  breast  milk  of  good  quality,  and 
those  over  three  months,  he  recommends  the  following  substitutes: 

1.  Heat  barley  flour  in  a  double  boiler,  the  water  in  the  outer  vessel 
to  be  kept  boiling  for  five  to  seven  days,  to  burst  the  starch  granules 
(Robinson's  prepared  barley  flour  can  be  bought). 

2.  Take  of  this  flour  one  tablespoonful,  add  25  or  30  tablespoon- 
fuls  of  boiling  water,  and  boil  and  mix  for  five  minutes.  Cool  to 
blood  heat,  add  1  dram  of  diastase  to  change  the  starch  to  dextrin 
and  maltose.  Forbes'  diastase  or  Taka-diastase  can  be  bought.  Of 
the  latter,  1  grain  will  change  150  grains  of  starch  to  sugar. 

Pasteurize  milk  by  heating  for  twenty  minutes  to  160°  F.  Cool 
quickly  on  ice  and  let  the  cream  separate.  To  two  and  one-half 
ounces  of  the  upper  half,  add  a  little  peptogenic  milk  powder  (Fair- 
child's),  to  peptonize  it.  He  mixes  the  peptonized  milk  with  three 
and  one-half  ounces  of  the  dextrinized  gruel  at  a  meal,  and  feeds 
the  infant  nine  or  ten  times,  at  two-hour  intervals.  Before  feeding, 
administer  a  few  drops  of  a  digestive  ferment. 

For  use  in  emergency,  he  recommends  two  heaped  teaspoonfuls 
of  condensed  milk  to  fifteen  teaspoonfuls  of  boiled  water,  as  equiva- 
lent to  seventeen  teaspoonfuls  of  ordinary  milk. 

He  gives  the  following  table  of  quantities  of  food  required  by 
infants;  either  breast  or  modified  cow's  milk  to  be  used. 


At  each  feeding. 
During  the  first  week 
At  the  third  week     . 
At  the  sixth  week     . 
At  the  third  month 
At  the  fourtli  month 
At  the  sixth  month  . 
At  the  tenth  to  twelfth  month 


Number 

of 

Total  daily 

daily  feedi 

QgS. 

quantity. 

1 

ounce 

10 

10  ounces 

u 

ounces 

10 

15 

2 

8 

16       " 

3 

8 

24       " 

4 

7 

.  28       " 

6 

6 

36       " 

8 

5 

40       " 

White,  following  Starr,  gi\'es  the  following  schedule  of  the  diet  of  a 
hand-fed  infant  from  birth  upward, ^  which  will  serve  as  a  suggestive 
and  useful  guide: 


1  Diseases  of  the  Digestive  Organs  in  Infancy  and  Childhood,  by  Louis  Starr,  M.D. 


PATHOLOGICAL  FIRST  DENTITION  2()<) 

Diet  During  the  First  Week. 

.      .      .  f3ii.i 

Cream jrr.  xv 

Sugar  of  milk '_  ^g^^^  f-y 

Whey f§gs_  f3ij 

This  p 'rlion  to  be  given>very  two  hours  from  5  a.m.  to  11  p.m.,  and  in  some  instances 
once  or  twice  during  the  night. 

Diet  from  the  Second  to  the  Fifth  Week. 

.      .      .  f§ss 

Milk ;      .      .      .  f3i,i 

Cream er.  xv 

Sugar  of  milk ^gj 

Water ,     ■      '.     '    . '  ^     1 1   „ ,, 

This  portion  to  be  given  every  two  hours  from  o  a.m.  to  11  i -M. 

Diet  from  the  Fifth  Week  to  the  End  of  the  Second  Month. 

,^.,,  fSJ.  f3i.i 

Milk ....  fSss 

Cream gj.   ^xx 

Sugar  of  milk ;  fgj,  f3ij 

Water 

This  portion  to  be  given  every  two  hours. 

Diet  During  the  Third  Month. 

.  fgiiss 

Milk ;  .  fgss 

Cream rz] 

Sugar  of  milk "      '      '       '  £g'j 

Water        .       .       •       ■ ,     ■       ■       ■       ',      '     ,'  ir  .      ' 
This  portion  to  be  given  every  two  and  one-halt  hours. 

Diet  During  the  Fourth  and  Fifth  Months. 

.     f  5  iiiss 
Milk ;      ;      .      .      .     fgss 


Cream 


3J 


Sugar  of  milk £gj 

Water 

This  portion  to  be  given  every  three  hours. 

Diet  During  the  Sixth  Month. 

foivss 

Milk fgss 

Cream gj 

Sugar  of  milk ^gj 

Water • 

This  portion  to  be  given  four  times  daily. 

Two  other  meals— morning  and  mid-day— may  be  as  follows: 


Milk 


fgivss 
foss 
3.i 


Cream 

Mellin's  Food ^gj 

mJTe  tie  Mellin's  Food  in  the  hot  water,  and  add',  with  stirring,'  to  the  previously 
mixed  milk  and  cream. 

In  the  seventh  month,  the  Mellin's  Food  ma>'  be  increased  to  two 
teaspoonfuls  and  given  three  times  daily. 
14 


210  DENTITION 

Throughout  the  eighth  and  ninth  months,  five  meals  a  day  will  be 
sufficient — at  7  and  10.30  a.m.,  2,  6,  and  10  p.m. 

Milk fgviss 

Cream       .      , fgss 

Sugar  of  milk 5.1 

Water fgj 

This  portion  for  the  first  and  last  meals. 

For  the  other  three  meals,  1  tablespoonful  of  Mellin's  Food  may  be 
added,  or  1  teaspoonful  of  "flour-ball"  may  be  given  twice  daily, 
instead  of  the  Mellin's  Food — say  at  the  second  and  fourth  meals. 

Diet  for  the  Tenth  and  Eleventh  Months. 

First  meal,  7  a.m.: 

Milk fgviiiss 

Cream fgss 

Mellin's  Food gss 

(Or  "flour-ball"  or  barley  jelly Sij) 

Water fgj 

To  be  used  only  when  Mellin's  Food  is  employed. 

Second  meal,  10.30  a.m.  :  Eight  ounces  of  warm  milk. 

Third  meal,  2  p.m.  :  The  yolk  of  an  egg  lightly  boiled  with  stale 
bread  crumbs. 

Fourth  meal,  6  p.m.  :  Same  as  first. 

Fifth  meal,  10  p.m.  :  Same  as  second. 

On  alternate  days  the  third  meal  may  consist  of  1  teacupful  (fSvj) 
of  beef  tea  containing  a  few  stale  bread  crumbs. 

Beef  tea,  for  an  infant,  is  made  in  the  following  way :  One-half  pound 
of  fresh  rump  steak,  free  from  fat,  is  cut  into  small  pieces,  and  put 
with  1  pint  of  cold  water  into  a  covered  tin  saucepan.  This  must 
stand  by  the  side  of  the  fire  for  four  hours,  then  be  allowed  to  simmer 
gently  (never  boil)  for  two  hours,  and,  finally,  be  thoroughly  skimmed 
to  remove  all  grease. 

A  further  variation  can  be  made  by  occasionally  using  mutton, 
chicken,  or  veal  broths  instead  of  beef  tea. 

DIET   FEOM   the   TWELFTH   TO   THE    EIGHTEENTH   MONTH 
(five   MEALS   A   DAY) 

First  meal,  7  a.m.  :  A  slice  of  stale  bread  broken  and  soaked  in  a 
breakfastcupful  (f§  viij)  of  new  milk. 

Second  meal,  10  a.m.:  A  teacupful  of  milk  (f^vj)  with  a  soda 
biscuit  or  thin  slice  of  buttered  bread. 

Third  meal,  2  p.m.  :  A  teacupful  of  beef  tea  (fg  vj)  with  a  slice  of 
bread,  1  good  tablespoonful  of  rice,  and  milk  pudding. 


PATHOLOGICAL  FIRST  DENTITION  211 

Fourth  meal,  6  p.m.  :  Same  as  first. 

Fifth  meal,  10  p.m.:  One  tablespoonful  of  Mellin's  Food  with 
1  breakfastcupful  of  milk. 

To  alternate  with  this: 

First  meal,  7  a.m.  :  The  yolk  of  one  egg  slightly  boiled,  with  bread 
crumbs;  1  teacupful  of  new  milk. 

Second  meal,  10  a.m.:  A  teacupful  of  milk  with  a  thin  slice  of 
buttered  bread. 

Third  meal,  2  p.m.:  A  mashed  boiled  potato,  moistened  with  4 
tablespoonfuls  of  beef  tea;  2  good  tablespoonfuls  of  junket. 

Fourth  meal,  6  p.m.:  A  breakfastcupful  of  new  milk  with  a  slice 
of  bread,  broken  up  and  soaked  in  it. 

Fifth  meal,  10  p.m.  :  Same  as  second. 

The  fifth  meal  is  often  unnecessary,  and  sleep  should  not  be  dis- 
turbed for  it.  At  the  same  time,  should  the  child  awake  an  hour  or 
more  before  the  first  meal  time,  he  should  break  his  fast  upon  a  cup 
of  warm  milk,  and  not  be  allowed  to  go  hungry  until  the  set  breakfast 
hour. 

DIET   FROM   EIGHTEEN   MONTHS   TO    THE    END    OF   TWO    AND    ONE- 
HALF   YEARS    (four   MEALS   A   DAY) 

First  meal,  7  a.m.:  A  breakfastcupful  of  new  milk;  the  yolk  of 
one  egg  lightly  boiled;  two  thin  slices  of  bread  and  butter. 

Second  meal,  11  a.m.:  A  teacupful  of  milk  with  soda  biscuit. 

Third  meal,  2  p.m.:  A  breakfastcupful  of  beef  tea,  mutton  or 
chicken  broth,  a  thin  slice  of  stale  bread,  a  saucer  of  rice,  and  milk 
pudding. 

Fourth  meal,  6^.30  p.m.:  A  breakfastcupful  of  milk  with  bread 
and  butter. 

On  alternate  days : 

First  meal,  7  a.m.  :  Two  tablespoonfuls  of  thoroughly  cooked  oat- 
meal or  wheaten  grits,  with  sugar  and  cream;  1  teacupful  of  new 
milk. 

Second  meal,  11  a.m.  :  A  teacupful  of  milk  with  a  slice  of  bread  and 
butter. 

Third  meal,  2  p.m.:  One  tablespoonful  of  underdone  mutton, 
pounded  to  a  paste;  bread  and  butter,  or  a  mashed  potato  moistened 
with  good  plain  dish  gravy;  a  saucer  of  junket. 

Fourth  meal,  6.30  p.m.  :  A  breakfastcupful  of  milk,  a  slice  of  soft 
milk  toast,  or  a  slice  or  two  of  bread  and  butter. 

The  foregoing  schedule  must,  of  course,  be  regarded  as  an  average. 
Many  children  can  bear  nothing  but  milk  food  up  to  the  age  of  two 


212  DENTITION 

or  even  three  years,  and  provided  enough  be  taken,  no  fear  for  their 
nutrition  need  be  entertained.  The  rule  to  adopt  is,  if  a  child  be 
thriving  on  milk,  it  is  never  to  be  forced  to  take  additional  food, 
merely  because  a  certain  age  has  been  reached.  Let  the  healthy 
appetite  be  the  guide. 

The  following  is  recommended  by  Starr  as  a  modified  milk  diet, 
and  as  a  substitute  for  mother's  milk  while  weaning: 

Pasteurized  cream fSss 

Pasteurized  milk fgiiss 

Sugar  of  milk 5ss 

Water,  boiled • fgj 

Should  this  not  satisfy  the  infant,  increase  the  ingredients  (except  cream)  to  6,  8, 
or  12  ounces. 

Hare^  recommends  the  following  diet  list,  followed  in  his  hospital 
practice : 

DIET    FOR   A    CHILD    AGED    TWO    YEARS. 

Breakfast,  7.30  a.m.:  Milk.  The  lightly  boiled  yolk  of  an  egg; 
thin  bread  and  butter  (the  bread  to  be  one  day  old). 

Lunch,  11  A.M.:  Milk.    A  thin  slice  of  bread  and  butter. 

Dinner,  1.30  p.m.:  Beef  tea,  or  small  piece  of  minced  roast  beef 
or  mutton,  devoid  of  gristle.  One  well-mashed  potato,  moistened  with 
gravy.    Rice  and  milk. 

Supper,  6  p.m.  :  Milk.    Bread  and  butter. 

For  drink:  Boiled  or  filtered  water. 

DIET    FOR   A    CHILD    AGED    ONE    YEAR    (fIVE    MEALS   A   DAY). 

First  meal,  7  a.m.:  2  teaspoonfuls  of  grated  flour-ball  (prepared 
as  directed  below)  in  |  pint  of  milk. 

Second  meal,  10.30  a.m.:  ^  pint  of  milk  with  4  tablespoonfuls 
of  lime  water. 

Third  meal,  2  p.m.  :  The  yolk  of  one  egg,  beaten  up  in  1  teacupful 
of  milk. 

Fourth  meal,  5.30  p.m.  :  Same  as  the  first. 

Fifth  meal,  11  p.m.:  Same  as  the  second. 

Flour-ball  is  to  be  made  by  taking  one  pound  of  good  flour — 
unbolted,  if  possible — tie  it  up  tery  tightly  in  a  pudding-bag;  put  it 
in  a  pot  of  boiling  water  early  in  the  morning,  and  let  it  boil  until 
bedtime,  then  take  it  out  and  let  it  dry.  In  the  morning,  peel  ofi^  the 
surface  and  throw  away  the  thin  rind  of  dough,  and  with  a  grater, 

1  Practical  Therapeutics. 


PATHOLOGICAL  FIRST  DENTITION  213 

tiTatc  down  tJie  hard,  dry  mass  into  a  jjowder.  To  use  this,  take 
from  1  to  2  teaspoonfiils  of  the  powder,  rub  it  (lo^^•n  until  smooth 
with  a  tablespoonful  of  eold  milk,  and  add  1  tumblerful  of  hot  milk, 

stirring  it  well  all  the  time. 

/ 

DIET    FOR   A    CHILD   AGED    FROM   SIX   TO    TWELVE    MONTHS    (fIVE 
MEALS    A    day). 

First  meal,  7  a.m.:  Mellm's  Food,  1  tablespoonful;  or  flour-ball 
grated,  1  or  2  teaspoonfuls  (prepared  as  directed  above) ;  hot  water, 
4  tablespoonfuls;  warm  milk,  enough  to  make  |  pint.  Dissolve  the 
Mellin's  Food,  or  rub  down  the  grated  flour-ball  in  the  hot  water  by 
stirring,  then  add  the  milk;  mix  thoroughly. 

Second  meal,  10.30  a.m.,  and  third  meal,  2  p.m.:  A  breakfast- 
cupful  of  milk,  W'ith  4  tablespoonfuls  of  lime  water. 

Fourth  meal,  5.30  p.m.  :  Same  as  first. 

Fifth  meal,  10.30  p.m.:  Same  as  second. 

Treatment  of  Nervous  ConditiOxVS. — If  nervous  reflexes,  great 
irritability,  or  cerebral  congestion  appear,  attention  should  be 
directed  to  the  condition  of  the  bowels  and  the  teeth. 

If  constipation  or  diarrhea  exist,  a  cathartic  is  given  and  the  gums 
are  lanced.    Ji  cerebral  sedative  is  to  be  prescribed. 

I^ — Chloralis  hydratis gr.  ij 

Sodii  bromidi gr.  v 

Aquae  menthae  piperitse f3ij — M. 

Sig. — Per  orem.     One  dose;   enlarge  formula  for  repetition  as  needed. 

If  convulsions  be  threatened,  the  clothing  should  be  loosened  and 
cool  applications  made  to  the  head. 

If  the  child  be  in  convulsions,  it  should  be  immersed  to  the  waist 
in  water  as  hot  as  can  be  borne,  to  which  has  been  added  2  table- 
spoonfuls of  common  mustard  flour,  and  cool  water  poured  over  its 
head,  when,  as  a  rule,  the  symptoms  promptly  subside.  Chloroform, 
which  children  endure  well,  may  be  administered. 

After  immersion,  a  rectal  injection  of  1  dram  of  glycerin  or  a 
glycerin  suppository  will  usually  cause  a  free  stool.  A  cerebral 
sedative  should  be  administered. 

I^ — Chloralis  hydratis    .       . gr.  ij 

Sodii  bromidi gr.  v 

Starch  paste gij — M. 

Sig. — To  be  administered  per  rectum.      (Atkinson.) 

It  is  wefl  also  to  administer  a  cathartic,  to  unload  the  intestines  of 
irritating  substances  possibly  present. 


214  DENTITION 

After  sleep,  if  appearances  indicating  dental  irritation  be  observed, 
gum  lancing  is  practised.  It  is  wise  that  this  operation  be  thus 
deferred,  as  convulsions  may  be  precipitated  by  the  act  of  lancing 
when  the  nervous  system  of  the  child  is  overexcited.  The  removal  of 
intestinal  irritants,  by  a  cathartic  given  per  orem  is  also  in  order, 
before  lancing. 

It  has  been  repeatedly  noted  that  when  evidence  of  marked 
cerebrospinal  irritation  is  present,  for  which  no  probable  source  can 
be  assigned,  and  an  examination  of  the  gums  shows  no  apparent  local 
disturbance,  yet  if  it  be  at  a  period  when  one  or  more  teeth  are  in 
process  of  eruption,  but  are  still  covered  or  bound  down  by  gum 
tissue,  if  gum  lancing  be  practised,  relief  is  immediate  and  the  lancing 
may  even  avert  a  threatened  attack  of  eclampsia.  It  is  presumed  that 
these  are  cases  of  pulp  irritation,  in  which  a  failure  of  resorption  of 
tissue  in  advance  of  the  tooth  crown  has  caused  pressure  upon  the 
pulp  forming  the  root  end. 

CONSTITUTIONAL   STATES   MODIFYING   DENTITION. 

Children  who  are  the  victims  of  hereditary  syphilis,  usually  cut 
their  teeth  very  early;  the  alveolar  process  being  in  many  cases 
insufficient.  Cases  are  recorded  where  children  have  been  born  with 
crowns  of  teeth  visible  upon  the  gum,  there  being  no  evidence  of  root 
formation,  the  crowns  being  loosely  held  to  the  gum  by  fibrous 
tissue.  It  is  necessary  to  remove  these  loose  crowns,  to  permit  the 
infant  to  suckle.  Children  affected  with  rachitis  have  the  process 
of  eruption  much  delayed.  It  is  seen,  therefore,  that  the  presence  of 
loose  crowns  of  teeth  is  a  condition  pointing  to,  though  by  no  means 
diagnostic  of,  hereditary  syphilis.  Long-delayed  eruption  of  teeth 
should  prompt  a  search  for  further  indications  of  rachitis.  Particu- 
larly in  children  in  whom  a  history  of  hereditary  syphilis  is  obtainable, 
the  process  of  dentition  may  be  accompanied  by  rapid  and  frequently 
widespread  breaking  down  of  the  soft  tissues,  over  and  about  erupting 
teeth.  Local  measures  of  treatment  seem  to  be  of  but  little  avail, 
except  that  antiseptic  treatment  undoubtedly  prevents  complications 
from  extraneous  infection. 

In  children  classified  indefinitely  as  strumous,  which  may  mean  the 
children  of  syphilitic  or  tuberculous  parents,  or  those  with  no  such 
history  whose  surroundings  are  of  the  most  unhygienic  kind,  the 
process  of  dentition  may  not  only  have  an  untoward  course,  but 
phagedenic  ulcerations  may  occur.  It  is  usually  in  the  degree  of  a 
child's  debility,  either  inherited  or  acquired  through  improper  care, 
that  dentition  assumes  morbid  features.    The  treatment  of  such  cases 


The  second  dentition  215 

must  be  directed  to  raising  the  health  standard.  As  local  therapeusis, 
no  measures  seem  more  effective  than  the  sprays  of  h}'drogen  dioxid 
first;  next,  potassium  chlorate,  and,  if  conditions  indicate  it,  sprays  of 
dilute  listerine,  which  is  stimulant,  antiseptic,  and  slightly  astringent. 

Infantile  Scurvy. — Cases  are  reported  in  which  the  improper 
feeding  of  children  has  been  followed  by  evidences  of  scorbutus.  It 
occurs  usually  in  bottle-fed  babies  confined  to  patent  foods,  the 
nutritive  element  being  lacking.  The  gums  become  tumid,  and 
hemorrhagic  extravasations  occur  in  their  substance;  the  periosteum 
is  stripped  from  the  margins  of  the  alveolar  walls,  the  soft  tissues 
hanging  in  discolored,  pendulous  masses  about  and  beyond  the  teeth 
if  any  be  erupted. 

The  child  is  peevish,  listless,  and  feeble.  There  is  apparent  pain 
in  the  limbs.^    The  urine  may  be  bloody  even,  as  a  first  sign. 

The  treatment  is  largely  systemic,  and  consists  of  using  fresh  cow's 
milk  modified  to  conform  to  human  milk,  and  in  the  administration 
of  fresh  lemon  juice,  preferably  boiled,  allowed  to  settle,  and  the 
supernatant  fluid  used,^  or  orange  juice  is  also  used. 

The  mouth  should  be  sprayed  with  sedative  antiseptics,  such  as 
potassium  chlorate  in  hydrogen  dioxid.     (See  p.  20;x) 


THE    SECOND    DENTITION. 

By  reference  to  Fig.  115,  it  will  be  seen  that  at  six  and  one-half  years 
of  age,  the  twenty  temporary  teeth  are  still  all  in  position,  and  that 
taking  their  places  in  the  line  of  the  arch,  are  the  four  permanent  first 
molars,  the  roots  of  which  are  still  incomplete. 

These  molars  do  not  replace  any  temporary  teeth,  but  during  the 
"change"  support  the  jaws  with  the  assistance  of  the  temporary 
molars  until  the  permanent  incisors  are  fully  erupted,  and  with  the 
aid  of  the  incisors,  until  the  bicuspids  come  into  occlusion.  Their 
office  as  jaw  props  and  organs  of  mastication  during  the  change  is, 
therefore,  very  important.  Of  their  later  function,  more  will  be  said 
farther  on. 

At  six  and  one-half  years,  the  crowns  of  the  permanent  incisors 
lie  in  the  relations  shown,  with  the  temporary  central  roots  resorbed 
and  the  lateral  root  partly  so.  Their  crowns  are  practically  complete, 
but  the  roots  are  unformed. 

The  cuspid  crown  in  its  crypt,  lies  well  above  and  lingual  to  the 
unresorbed  temporary  cuspid  root.    The  roots  of  the  first  and  second 

1  Hare.  ^  Ibid. 


216  DENTITION    . 

temporary  molars,  a  trifle  resorbed  upon  the  inner  side,  embrace  the 
formed  crowns  of  the  first  and  second  bicuspids. 

In  their  crypts  back  of  the  first  molars,  lie  the  forming  crowns  of 
the  second  permanent  molars.  The  third  molars  are  not  in  evidence 
in  the  illustration,  but  their  development  is  in  progress. 

It  will  be  seen  that  the  permanent  central  and  lateral  incisors 
replace  the  temporary  central  and  lateral  incisors,  the  permanent 
cuspid  the  temporary  cuspid,  and  the  first  and  second  bicuspids  the 
first  and  second  temporary  molars,  respectively. 

From  this  age  to  adult  age,  as  previously,  the  jaw  undergoes  constant 
change,  enlarges  by  constant  resorptions  and  depositions  of  bone,  and 
changes  its  contour  to  conform  to  the  changes  occurring  throughout 
the  body,  and  to  accommodate  the  permanent  teeth,  which  are  in 
general  terms  larger  and  more  numerous  than  the  temporary  teeth. 

It  may  be  said  that  the  alveolar  process  built  about  the  roots  of 
temporary  teeth  and  the  roots  of  the  temporary  teeth  are  all  resorbed 
during  the  replacement  of  the  latter,  and  that  when  the  crowns  of 
the  permanent  teeth  are  fully  erupted,  new  alveolar  process  is  built 
up  about  their  roots.  Any  subsequent  change  in  the  position  of  the 
permanent  teeth  is  accompanied  by  an  alteration  in  the  alveolar  pro- 
cess, and  after  extraction  the  latter  is  resorbed,  but  upon  an  implan- 
tation (which  see)  being  done,  new  process  will  form.  Its  dependence 
upon  the  teeth  is,  therefore,  evident. 

The  following  table  gives  the  approximate  ages  for  the  eruption 
of  the  permanent  teeth: 

First  molars 5^  to    7  years 

Central  incisors 7    to    8  years 

Lateral  incisors 8    to    9  years 

First  bicuspids ■  10    to  11  years 

Second  bicuspids 11     to  12  years 

Cuspids,  the  lower  usually  preceding  by  a  year  or  more  12    to  14  years 

Second  molars 12    to  15  years 

Third  molars 16    to  20  years 

and  indefinitely  beyond 

The  Process  of  Resorption  of  the  Temporary  Roots. — After  com- 
pletion of  formation,  the  roots  of  the  temporary  teeth  remain  in  this 
state  but  a  short  time,  as  their  successors  are  ready  to  advance  to 
their  places. 

Comparing  the  ages  at  which  resorption  begins  with  the  ages  at 
which  it  is  complete  (eruption  of  permanent  teeth)  (see  Fig.  146),  it 
will  be  noted  that  approximately  three  and  one-half  years  are  required 
in  all  cases  for  the  removal  of  the  temporary  roots.  Therefore,  to 
determine  the  age  at  which  absorption  begins,  deduct  three  and  one- 
half  years  from  the  date  of  eruption  of  the  corresponding  permanent 
tooth.    The  degree  of  resorption  at  any  age  is  shown  in  the  table. 


THE  SECOND  DENTITION 


217 


At  the  time  the  permanent  tooth  begins  its  advance,  it  hes  in  a 
bony  crypt  above  and  Hngnal  to  its  predecessor,  except  in  the  case 


Fig.   146 

k 


JLl   ,Jl1  ""ihl  „l\i  i  I  %  Iff 
r" m  ^ifi^m     w  ••mm  I l M  ^^  ji„*i.n,..,if 


Decalcification  of  the  deciduous  teeth.     The  numbers  indicate  years.      (Peirce.) 


Fig.  147 


Fig.  148 


Showing  the  relations  of  an  erupt- 
ing permanent  tooth  to  its  deciduous 
predecessor.  A,  A,  A,  odontoclasts 
in  absorbent  organ. 


The  structure  of  the  absoibent  organ, 
showing  multinucleated  or  giant  cells 
(odontoclasts).      (Tomes.) 

Fig.   149 


^^W  ^tt0^r 


Imprisonment  of  second  temporary 
molar;  resorption  of  its  roots,  with 
absence  of  second  bicuspid.  (Skiagraph 
by  Custer.) 


of  the  bicuspids,  which   He   between  the  roots  of   the   temporary 
molars  (Fig.  112  to  115). 


218 


DENTITION 


Each  crypt  has  its  own  folhcle  wall  enclosing  a  permanent  tooth 


crown. 


In  the  follicular  wall  overlying  the  crown,  appear  large  multinu- 
cleated cells,  the  origin  of  which  is  unknown,  but  which  by  some  are 
thought  to  be  transformed  osteoblasts,  by  others  leukocytes  (Figs. 
147  and  148).  The  latter  is  the  probable  explanation,  as  analogous 
cells  are  found  about  tissues  or  foreign  bodies  about  to  undergo 
resorption  anywhere  in  the  body.  (See  Resorption.)  In  the  par- 
ticular situation  under  consideration  they  are  called  odontoclasts. 
The  tissue  between  the  root  and  crown  has  by  Tomes  been  given 
the  name  of  the  "absorbent  organ"  (Figs.  147  A,  and  148).  These 
giant  cells  have  a  solvent  or  digestive  function  not  understood,  but 


Fig.   150 


Fig.  151 


Phases  of  resorption  of  temporary  roots. 
(Skiagraph  by  Price. i) 


Diagram  illustrating  the 
relation  of  a  resorbed  tem- 
porary root  and  the  perma- 
nent tooth, also  the  involve- 
ment of  the  pulp  as  a  part 
of  the  resorbent  organ. 
Resorption  of  the  interior 
of  crown  of  a  temporary 
tooth.     From  actual  case. 


which  is  competent  to  remove  both  the  organic  and  inorganic  matter 
of  cementum  and  dentin,  and  evidences  of  action  upon  enamel  in 
other  situations  are  not  wanting.  (See  Resorption  of  Enamel.) 
That  the  solvent  is  acid,  is  shown  by  the  evidence  of  decalcification 
about  the  area  of  resorbed  enamel  of  unerupted  crowns  of  some 
permanent  teeth.  It  is  a  curious  fact  that  no  evidence  of  decalci- 
fication of  the  permanent  crown  has  been  demonstrated  to  result 
from  the  proximity  of  the  multinucleated  cells  in  cases  of  physio- 
logical resorption  of  roots.  In  all  probability  the  enamel  is  pro- 
tected by  the  presence  of  Nasmyth's  membrane,  which  is  resistant 


1  Items  of  Interest,  1901. 


THE  SECOND  DENTITION  219 

to  acids.  These  cells  are  probably  invited  by  irritation  due  to 
pressure  of  the  advancing  permanent  tooth  crown,  as  the  resorption 
is  almost  always  found  at  the  point  of  approximation  of  the  crown 
with  the  root,  or,  in  other  words,  at  the  pressure  point  (Fig.  150). 

Cases  of  resorption  of  temporary  roots  without  the  presence  of  a 
permanent  crown  are,  however,  noted  and  explained  by  Tomes 
upon  the  ground  that  resorption  is  a  vital  act  independent  of  the 
pressure  exerted  (Fig.  149).  As  resorption  of  permanent  roots, 
however,  has  often  occurred  from  pressure  of  the  crown  of  another 
tooth  and  occurs  at  the  pressure  point  in  physiological  resorption, 
localized  irritation,  even  in  the  absence  of  a  permanent  crown,  must 
be  credited  with  a  large  influence  in  the  process.  It  is  to  be  remem- 
bered also  that  in  the  absence  of  the  pressure,  resorption  often  does 
not  occur,  at  least  for  twenty-five  or  more  years — e.  g.,  when  laterals 
are  absent  and  the  permanent  cuspids  erupt  to  the  side  of  the 
deciduous  cuspids  (Fig.  153). 

According  to  Tomes,  redeposition  of  cementum  occurs  in  pre- 
viously resorbed  areas  upon  temporary  roots;  a  fact  corresponding 
with  effects  noted  in  permanent  roots. 

Teeth  frequently  erupt  lingually  or  labially  to  their  corresponding 
temporary  teeth,  both  remaining  in  the  mouth.  It  is  almost  invari- 
ably the  rule,  upon  extraction  to  find  that  an  oblique  resorption  has 
occurred,  as  is  shown  in  the  right  upper  skiagraph  in  Fig.  150,  and 
generally  a  decided  hyperemia  is  seen  in  the  pulp  extending  upward 
for  perhaps  a  quarter  of  an  inch. 

Doskow^  has  shown  by  the  prompt  loss,  by  absorption,  of  a  fairly 
firm  deciduous  cuspid,  crowned  to  bring  it  up  to  level  and  so  to 
usefulness,  that  such  an  operation  is  inadvisable  because  of  an  inher- 
ent tendency  of  an  absorbent  organ  to  become  established.  Again, 
a  permanent  tooth  undergoing  resorption  often  remains  firm,  until 
suddenly  the  strain  becomes  too  great. 

As  the  root  of  the  temporary  tooth  disappears,  the  pulp  continu- 
ously fuses  with  the  absorbent  organ,  so  that  when  the  crown  alone 
remains,  the  pulp  is  still  vital  (Figs.  147  and  151).  At  times,  it  seems 
to  take  up  the  resorbent  function  and  resorbs  the  crown  dentin  in 
some  cases  almost  entirely.  In  one  specimen,  a  circumscribed  portion 
of  the  cementum  and  of  enamel  were  removed  by  it,  at  the  point  of 
junction.  This  constituted  practically  a  case  of  perforation  by 
resorption  (Fig.  151).  The  tooth  was  at  first  thought  to  be  suft\ised 
with  hemoglobin,  as  it  was  of  a  pink  color.  After  extraction  the 
absorbent  organ  was  found  as  a  papilla  attached  to  the  gum.     At 

1  Dental  Cosmos,  1907. 


220 


DENTITION 


times,  bay-like  excavations  in  the  crown  dentin  occur  (Fig.  209,  D). 
When  the  root  resorption  reaches  the  point  shown  in  the  central 
incisor  in  Fig.  115  the  temporary  tooth  is  loosened,  moves  about,  and 
annoys  the  child,  who  may  pick  it  out,  or  it  is  removed  by  extraction. 
Formation  of  the  Roots  of  Permanent  Teeth. — The  extent  of  root 
development  at  any  age  is  of  great  importance  in  view  of  canal  thera- 
peutics. Incomplete  roots  present  a  mechanical  difficulty  of  sealing 
the  apex  of  the  canal.  The  size  of  the  pulp  at  the  apical  foramen 
of  such  teeth  contraindicates  the  use  of  arsenic,  and  even  pressure 
anesthesia  is  often  unsuccessfully  applied. 

Fig.  152 


Absence  of  upper  left  lateral  incisor,  with  permanent  cuspid  in  its  place;    two 
temporary  cuspids  retained.      Man,  aged  twenty-five  years. 


The  roots  are  developed  in  precisely  the  same  manner  as  in  the 
case  of  the  temporary  teeth,  by  the  combined  deposition  of  cementum 
by  the  osteogenetic  cells  of  the  follicular  wall,  which  is  drawn  up  on 
the  root  as  a  pericementum,  and  by  the  odontoblasts  of  the  papilla, 
which  is  drawn  up  as  a  pulp  (Fig.  110). 

The  extent  of  development  of  any  of  the  permanent  teeth  may  be 
seen  at  a  glance  by  reference  to  the  valuable  table  of  Peirce  (Fig.  116). 
So  graphically  does  this  table  give  the  desired  information  that 
explanation  becomes  unnecessary. 

Irregularities  of  Second  Dentition. — Some  temporary  teeth  may 
be  retained  long  after  adult  age  is  reached.  The  teeth  most  subject 
to  this  are  the  cuspids  and  second  temporary  molars. 


THE  SECOND  DENTITION 


221 


In  the  case  of  the  cuspids,  the  permanent  cuspid  is  delayed  or 
takes  an  unusual  direction,  erupting  lingually  or  labially,  or  at  times 
being  directed  into  the  place  normally  occupied  by  the  lateral 
incisors,  which  are  wanting,  or  very  rarely,  the  cuspid  erupts  pos- 
teriorly to  the  first  bicuspid.  At  about  forty  years  of  age,  the  tem- 
porary cuspids  may  be  lost  by  resorption  of  their  roots,  but  until 
such  time  should  be  retained  if  usefully  filling  a  space.  If  in  inter- 
ference with  proper  alignment  or  eruption  of  the  permanent  cuspid, 
they  should  be  extracted.  Their  late  resorption  is  somewhat  patho- 
logical in  character,  and  probably  due  to  or  incited  by  a  partial 
resorption  of  the  root  end  during  the  descent  of  the  permanent 
cuspid. 


Fig.   1.53 


Absence  of  upper  lateral  incisors  and  right  bicuspid.    Retention  of  temporary  cuspids. 

From  an  adult. 


The  late  enforced  loss  of  the  temporary  cuspid  indicates  the 
advisability  of  an  implantation  operation  (Fig.  153). 

The  molars  are  retained,  as  a  rule,  because  of  an  absence  of  per- 
manent crowns  to  cause  resorption,  although  this  may  occur  without 
such  pressure  (Fig.  149).  I  have  seen  a  case  of  an  adult  lady  with 
eight  deciduous  molars  in  place.  The  question  of  the  abnormal  de- 
velopment or  absence  of  permanent  germs,  or  of  the  state  of  the 
roots  of  the  temporary  tooth  may  be  settled  by  the  a'-rays  (Figs.  150 
and  154). 

The  question  of  extraction  or  retention  depends  upon  the  diag- 
nosis.   A  firm  temporary  tooth  should  never  be  extracted  simply  to 


222 


DENTITION 


Fig.  154 


allow  a  permanent  tooth  to  erupt  unless  the  presence  of  a  permanent 
tooth  in  the  jaw,  as  determined  by  skiagraph  or  other  means,  gives 
reasonable  inference  that  the  permanent  tooth  is  held  back  by  the 
temporary  tooth.  In  most  cases  a  reasonable  delay  is  advisable. 
A  patient  of  the  editor  wore  a  plate  for  thirteen  years  because  of  the 

injudicious  extraction  of  an  upper 
temporary  cuspid,  the  permanent 
tooth  appearing  at  twenty-six  years 
of   age. 

When  the  retention  of  temporary 
molars  and  cuspids  occurs,  they  are 
apt  to  occupy  an  occlusal  level,  lower 
than  that  of  the  permanent  teeth 
(Fig.  149).  They  may  not  be  in 
occlusion  at  all,  as  was  the  case  with 
the  eight  molars  just  referred  to. 
This  proves  the  fact  that  the  gener-al 
occlusal  level  of  the  permanent  teeth 
is  farther  from  the  margin  of  the  alveolar  process  than  in  the  case  of 
the  temporary  teeth.  The  length  of  the  permanent  crowns  accounts 
for  this.  In  normal  replacement,  however,  the  occlusal  level  is  nearly 
the  same  for  the  temporary  molars  and  first  permanent  molar,  at 
least  until  the  change  is  made  by  the  eruption  of  the  bicuspid. 


Retained  temporary  molar  with  bi- 
cuspid present.  (Skiagraph  by  E 
Ballard  Lodge.) 


Fig.   155 


Fig.  156 


Retained  lower  temporary  molars,  bi- 
cuspid absent.  (Skiagraph  by  E.  Ballard 
Lodge.) 


Delayed    cuspid.       (Skiagraph    by    E. 
Ballard  Lodge.) 


The  correct  placement  of  these  first  permanent  molars  seems  to 
determine  the  correctness  of  molar  occlusion,  at  least  in  the  mesio- 
distal  relation,  though  they  may  not  occupy  their  correct  bucco- 
lingual  positions.  Any  slight  forces  disturbing  the  mesiodistal 
relation,  causing  the  upper  first  molar  to  drift  anterior  to  its  correct 


THE  SECOND   DENTITION 


223 


occlusion  with  the  lower  molar,  will  result  in  an  abnormal  relation 
of  the  teeth  to  those  anterior  to  them  and  to  their  antagonists ;  either 
upper  protrusion  or  upper  irregularities  will  occur. 

If  the  reverse  occur,  and  the  lower  molar  be  placed  anteriorly,  and 
the  upper  be  placed  normally  or  posterior  to  its  normal  position, 
prognathism  of  the  lower  teeth  ordinarily  results.  If  placed  too  far 
posteriorly,  retrusion  of  the  lower  teeth  will  occur. 

Fig.  157 


Typical  occlusion.      (Cryer.) 


According  to  Angle,  the  misplacement  of  the  permanent  teeth 
erupting  early  causes  their  inclined  planes  to  direct  other  teeth  from 
normal  occlusion,  or  by  permitting  contraction  of  the  space  normally 
occupied,  particularly  in  the  lower  jaw,  permits  the  other  teeth  to 
assume  a  position  in  a  contracted  arch,  thus  again  causing  their 
inclined  planes  to  cause  contraction  in  the  opposite  arch,  with  a 
consequent  displacement,  buccolingually,  of  teeth  which  would  other- 
wise normally  align  themselves  in  the  arch.  Once  established,  the 
cheek  and  lip  pressure  maintains  the  inharmony  (Fig.  162). 

Angle  divides  all  irregularities  into  three  classes,  with  divisions 
and  subdivisions: 


224  DENTITION 

Class  I. — The  first  molars  are  correctly  occluded  mesiodistally, 
the  teeth  anterior  being  in  malocclusion,  though  the  biscuspids  may 
be  in  correct  mesiodistal  relation. 

The  general  characteristic  of  the  class  is  that  shown  in  Fig.  158. 

Fig.   158 


Malocclusion.     Class  I.      (Angle.) 

Class  II. — The  lower  first  molars  occlude  distally  to  the  upper 
first  molars,  causing  retrusion  of  the  lower  jaw.  Division  I  is  char- 
acterized by  distal  occlusion  on  both  sides,  the  upper  arch  is  narrowed, 
the  upper  incisors  lengthened  and  protruded.  The  upper  lip  is  short 
and  functionless,  while  the  lower  lip  is  thickened  and  rests  cushion- 
like between  the  upper  and  lower  incisors,  increasing  the  protrusion 
of  the  upper  and  the  retrusion  of  the  lower.  There  is  usually  mouth 
breathing,  due  to  some  form  of  nasal  obstruction. 

Division  I. — The  characteristic  exists  on  one  side  only,  the  other 
being  normal.    Mouth  breathing  is  usually  associated  (Fig.  159). 

Division  II. — There  is  distal  occlusion  on  both  sides,  but  the 
upper  incisors  are  retruded  instead  of  protruded,  with  crowding  in 
the  cuspid  region.  These  are  associated  with  normal  breathing 
(Fig.  160). 


THE  SECOND  DENTITION 


225 


Subdivision,  Division  II. — The  characteristic  is  upon  one  side 
only,  normal  breathers. 

Class  III  — Division  I. — In  this  class,  the  lower  first  molars  occlude 
mesially  to  the  upper  first  molars  on  both  sides,  and  the  lower  jaw 
progressively  protrudes  anteriorly  (Fig.  161). 

-    Fig.   159 


Malocclusion.     Class  II.      (Angle.) 


Subdivision,  Class  III. — The  mesial  occlusion  is  upon  one  side 
only,  the  other  being  normal,  the  arches  crossing  in  the  region  of  the 
incisors. 

Angle  has  formulated  the  law  "that  the  best  balance,  the  best 
harmony,  the  best  proportions  of  the  mouth  in  its  relations  to  the 
other  features  require  that  there  shall  be  the  full  complement  of 
teeth,  aftd  that  each  tooth  shall  be  made  to  occupy  its  normal 
occlusional  relations.  He  also  states  that  the  best  development  of 
the  bones  of  the  face  and  throat,  the  size  and  function  of  its  cavities 
are  dependent  upon  the  position  of  the  teeth. 

The  specific  causes   inducing  malocclusion  of  the  teeth  as  classi- 
fied above  are: 
15 


226 


DENTITION 

Fig.   160 


Malocclusion.     Class  II.     Division  II.      (Angls.) 
Fig.   161 


Malocclusion.     Class  III.     (Angle.) 


THE  SECOND  DENTITION 


227 


Fig.   162 


1.  Premature  loss  of  deciduous  teeth  prevents  the  pressure  of  the 
first  molars  upon  the  teeth  anterior  to  them,  which  mechanically  aids 
in  the  development  of  the  jaws  and  thus  of  the  space  necessary  for 
accommodation  of  the  permanent  teeth.  It 
also  allows  the  first  molar  to  drift  forward  and 
come  into  malocclusion,  and  also  to  close  the 
space  occupied  by  the  deciduous  tooth,  thus 
lessening  space  for  its  successor  and  forcing  it 
into  buccal  or  lingual  displacement.  The  same 
is  true  of  loss  of  approximal  tooth  contact  as 
the  result  of  caries  (Fig.  162). 

2.  Prolonged  retention  of  deciduous  teeth 
may  cause  a  deflection  of  the  temporary  suc- 
cessor or  prevent  its  eruption. 

3.  Through  loss  of  permanent  teeth  on  that 
side   upon  which   the    tooth  is  extracted,   the 

development  of  the  jaw  will  be  prevented  and  the  tooth  posterior  to 
the  space  will  tend  to  tip  or  drift  forward  into  malocclusion. 


Effects  of  the  prema- 
ture loss  of  a  deciduous 
second  molar. 


Fig.   163 


Fig.  164 


Case  of  adenoids.     Fig.  163,  before  operation;     Fig.  164,  after  operation.     (Faught.) 


4.  Tardy  eruption  of  permanent  teeth  permits  closure  of  the  space 
altogether  or  in  part,  and  the  resistance  offered  causes  a  deflec- 
tion of  the  tardy  tooth  (Fig.  162).  The  total  absence  of  certain 
permanent  teeth  may  be  placed  under  this  heading. 

5.  Supernumerary  teeth,  by  occupying  space,  also  compel  the 
normal  teeth  to  take  an  abnormal  position,  and,  if  erupting  after 
them,  may  displace  them  by  constant  pressure  (Figs.  220  and  250). 


228 


DENTITION 


6.  Habits  such  as  thumb  and  lip  sucking  or  lip  biting  will  move  the 
upper  anterior  teeth  outward  and  the  lower  anterior  teeth  inward. 


Fig.   165 


Fig.  166 


Diagrammatic  sagittal  section,  show- 
ing relation  of  anatomical  landmarks. 
(Faught.) 

Fig.   167 


Adenoid    vegetations.        Compare    Fig. 
165.     (Faught.) 


Diagrammatic  coronal  section  through  head  in  the  region  of  the  first  rholar,  show- 
ing nasal  septum,  uncinate  process,  inferior  meatus,  inferior  turbinals,  middle  ethmoidal 
cells,  middle  turbinates,  and  hiatus  semilunaris.      (Faught.) 


Holding  the  tongue  between  the  anterior  teeth  produces  infra- 
occlusion  of  the  anterior  teeth,  while  the  constantly  open  mouth  per- 
mits supra-occlusion  of  the  molars. 


THE  SECOND  DENTITION  229 

7.  Nasal  obstructions  occurring  in  the  developing  child  produce 
mouth  breathing,  and  the  opening  of  the  mouth  causes  contraction 
of  the  muscles  upon  the  teeth  and  bones,  producing  abnormalities 
of  the  bone  of  the  jaw;  the  irregularity  of  Class  II  (Division  I),  an 
undeveloped  nose  and  adjacent  region  of  the  face.    Faught  has  ably 

Fig.   168 


Hypertrophy  of  right  inferior  turbinal,  also  deflected  septum  and  spur. 
Compare  Fig.  167.      (Faught.) 

Fig.  169 


Cystic  middle  turbinal,  hypertrophied  inferior  turbinals,   enlarged  middle   ethmoidal 
cells,  and  hypertrophied  middle  turbinal.     Compare  Fig.  167.      (Faught.) 

illustrated  these  conditions  in  Figs.  163  to  171. ^  The  consideration  of 
malocclusion  as  a  general  subject  is  properly  relegated  to  special 
works,  and  the  reader  is  referred  to  Angle's  Malocclusion  of  the  Teeth 
and  other  works  on  the  subject. 

1  Dental  Cosmos,  1908,  p.  7. 


230  DENTITION 

Disorders  of  the  Second  Dentition. — The  devitahzation  of  the 
pulp  of  a  temporary  tooth  and  proper  canal  filling  delays,  but  does  not 
absolutely  prevent,  resorption.     Chronic  abscesses  upon  such  roots 

Fig.  170  Fig.  171 


Hypertrophied  posterior  end  of  inferior  Nasal  polypi.     Compare  Fig.  165. 

turbinal.  Compare  Fig.  165.    (Faught.)  (Faught.) 

Fig.   172 


Right.  ■  Left. 

Labial  aspect  of  bilateral  sequestra  apparently  due  to  typhoid  fever  alone.     (Cowper.) 

destroy  the  absorbent  organ,  but  some  pathological  resorption  may 
occur,  as  in  case  of  permanent  roots  (which  see) .  Pus  has  an  alkaline 
reaction  which  may  neutralize  the  acid  solvent.  As  a  rule,  such  roots 
are  mechanical  obstructions  to  the  permanent  crowns,  which  are 


THE  SECOND  DENTITION  231 

deflected  to  one  side  and  caused  to  erupt  irregularly;  again,  the 
temporary  root  may  be  bodily  pushed  aside,  its  apex  pressed  against 
the  alveolar  process  and  gum  tissue,  which  are  resorbed,  and  the 
necrotic  root  end  is  seen  extruded  through  the  gum.  Extraction  is 
indicated. 

When  temporary  roots  are  not  thus  mechanically  removed  they  are 
gradually  extruded  and  decayed,  or  suppurative  processes  cause  the 
resorption  of  the  alveolar  process  about  them. 

Injudicious  retention  of  temporary  teeth  may  thus  cause  an  irregu- 
larity. On  the  other  hand,  premature  extraction  by  permitting  the 
approximation  of  the  previously  erupted  permanent  teeth  may  have 
an  equally  bad  effect  upon  an  erupting  tooth  (Fig.  162). 

In  anticipation  of  physiological  resorption  of  temporary  roots,  all 
temporary  teeth  should  be  carefully  watched,  cleansed,  filled,  and,  if 
necessary,  their  roots  treated  so  that  a  normal  replacement  by  the 
permanent  teeth  may  occur.  If  pronounced  disease  occur  just 
previous  to  the  time  for  normal  replacement,  extraction  is  indicated. 

Early  extraction  has  sometimes  caused  early  eruption  of  the  per- 
manent teeth,  e.  g.,  bicuspids  at  seven  years  of  age. 

It  will  be  recalled  that  the  teeth  are  an  evolution  of  the  dermoid 
system,  which  fact  possesses  pathological  significance  in  certain  acute, 
specific  skin  diseases.  It  is  noted  in  some  cases  of  the  eruptive 
fevers  of  children,  particularly  when  the  child  is  much  debilitated, 
that  after  the  cessation  of  the  acute  disease,  a  necrotic  affection  of 
the  jaw  occurs,  involving  the  alveolar  bone  and  its  contents.  As 
many  of  these  cases  occur  between  the  ages  of  three  and  seven  years, 
the  temporary  teeth  are  still  in  situ;  these,  with  the  partially  devel- 
oped permanent  teeth  and  the  enclosing  bone,  may  be  exfoliated. 
The  necrotic  process  may  involve  but  one  tooth,  or  may  include 
all  of  the  temporary  teeth,  their  successors,  and  a  large  mass  of 
bone.^  The  disease  with  which  this  necrosis  is  most  frequently 
associated  is  scarlet  fever  ;^  it  is  also  found  as  a  sequel  of  measles 
and  smallpox.  "The  cases  prior  to  exfoliation  of  the  bone,  exhibit 
a  stripping  of  the  periosteum,  apparently  beginning  about  the  necks 
of  the  teeth.  A  discharge  of  pus  having  a  fetid  odor  is  present,  and 
the  soft  tissues  may  be  raised  from  the  bone  for  a  variable  extent;" 
that  is,  there  is  evidence  of  purulent  periostitis.  In  the  course  of 
some  weeks,  six  or  eight,  the  necrotic  bone  and  its  contents  exfoliate. 
Salter  observes  that  the  sequestra  forming  after  severe  scarlet  fever 
are  much  more  extensive  than  those  which  form  as  a  sequel  of  measles. 

An  interesting  case  of  bilateral  sequestra  of  the  aveolar  process 

1  Salter,  Dental  Pathology.  ^  Ibid. 


232  DENTITION 

due  to  typhoid  fever  alone  is  reported  by  Cowper.^  Two  sound 
teeth  were  involved  in  each  sequestrum.      (Fig.  172.) 

The  administration  to  children,  of  mercurials,  has  caused  such  a 
loss  of  teeth  and  process.  I  have  seen  a  sequestrum  containing  three 
undecayed  teeth  attributed  to  this  cause,  and  others  have  been 
reported.  In  these  cases  the  parts  should  be  kept  as  aseptic  as 
possible  by  means  of  hydrogen  dioxid  and  the  compound  tincture 
of  capsicum  and  myrrh  (enough  to  cloud  a  glass  of  water),  used  as  a 
stimulant  mouth  wash.^  When  loose,  the  sequestrum  should  be 
removed.  The  parts  heal  by  granulation,  if  due  attention  be  paid 
to  the  general  physical  welfare  of  the  child. 

Eruption  of  the  Molars. — The  first  permanent  molars  rarely 
produce  more  than  slight  rheumatic  pains.  The  gum  irritation 
may  be  relieved  by  an  X-incision,  or  at  times  by  the  application 
of  phenol-sodique  and  laudanum,  equal  parts,  or  phenol  camphor, 
with  the  finger  tip.  A  little  alcohol  or  dilute  tincture  of  iodin  serves 
almost  equally  well. 

As  some  time  may  elapse  between  eruption  and  occlusion,  the  first 
molars  do  not  receive  a  proper  friction.  Associated  frequently  with 
carious  temporary  teeth,  they  are  frequently  decayed  in  their  sulci 
and  fissures;  to  prevent  this  it  has  been  recommended  that  oxy- 
phosphate  of  zinc  be  placed  over  these  fissures  without  previous 
excavation.^  The  oxyphosphate  of  zinc  or  copper  may  also  be  thus 
used  in  third  molars  which  are  even  more  liable  to  dental  caries. 

The  lower  second  molars  may  cause  some  irritation  owing  to  an 
insufficient  development  of  the  jaw  at  the  angle,  leaving  an  inade- 
quate accommodation  for  the  crown.  At  about  nine  years  of  age 
the  second  molar  occupies  the  angle  of  the  jaw  in  much  the  same 
position  as  shown  in  Fig.  Ill  for  the  third  molar.  If  held  back,  a 
pathological  condition  equivalent  to  that  occurring  in  the  temporary 
teeth  may  result;  reflexes  producing  heavy  pains  about  the  jaw  or 
reflex  effects,  such  as  chorea,  may  be  produced. 

Truman^  has  prevented  a  threatened  second  attack  of  this  sort  by 
deep  incisions  in  the  gum  over  the  site  of  the  crown.  The  presump- 
tion is  that  such  treatment  relieves  the  tension  upon  the  pulp  under- 
lying the  developing  root. 

Kirk^  calls  attention  to  the  liability  of  chorea  to  be  associated  with 
reflexes  from  the  dental  region  at  from  four  to  nine  years  of  age,  and 
cites  a  case  from  the  practice  of  C.  N.  Peirce  in  which  choreic  mani- 
festations were  permanently  relieved  by  the  removal  of  a  deciduous 

1  Dental  Cosmos,  1909,  p.  765.  2  Garretson,  A  System  of  Oral  Surgery. 

3  L.  Ashley  Faught.  ^  International  Dental  Journal,  1899. 

6  Dental  Cosmos,  1905. 


THE  SECOND  DENTITION  233 

molar  interfering  with  the  eruption  of  its  permanent  successor,  the 
bicuspid.  He  also  cites  a  case  of  repeated  hysterical  manifestations, 
following  nervous  irritability  due  to  each  replacement  of  a  deciduous 
tooth  by  its  successor.  Flagg  cured  a  case  of  chorea  in  a  boy,  by 
the  extraction  of  four  teeth  from  a  very  crowded  arch.^ 

The  third  molars  frequently  induce  pathological  conditions. 

The  upper  third  molar,  meeting  in  its  descent  the  roots  of  the 
second  molar,  may  be  united  to  it  by  hypercementosis — the  condition 
of  concrescence  (which  see) ;  escaping  this,  it  may  meet  a  dense  palato- 
alveolar  plate  of  bone  at  the  tuberosity  and  be  deflected  buccally 
through  the  thinner  buccal  plate  of  bone,  so  that  its  occlusal  face 
presents  cheekward  (Fig.  173).  Its  occlusal  face  may  present  more 
posteriorly  or  more  anteriorly.  Here  retained  food  collects  about 
it  and  caries  occurs,  or  a  suppurative  inflammation  of  the  cheek 
or  free  gum  margin  may  occur.    For  this  condition  sterilization,  free 

Fig.  173  Fig.  174 


Abnormal  eruption  of  the  upper  third  Partial  eruption  and  impaction  of  third 

molar.  molar.     (Skiagraph  by  Custer.) 


incision  of  the  gum  margin,  and  subsequent  asepsis  maintained  by 
antiseptic  sprays  will  reduce  the  inflammation,  which,  however,  is 
apt  to  recur  at  intervals.  If  the  cheek  be  irritated  or  the  position  of 
the  tooth  permanently  fixed,  only  traction  of  the  tooth  into  a  correct 
position,  grinding  away  of  the  sharp  cusps,  or  extraction  wdll  alle- 
viate the  condition.  The  extraction  of  such  a  tooth  is  little  loss  to  the 
individual.  A  bit  of  cotton  saturated  with  a  mild  antiseptic  may 
be  placed  between  the  tooth  and  cheek  for  a  time  after  grinding. 
The  possibility  of  concrescence  in  such  a  case,  as  shown  in  Fig.  173, 
must  be  considered  when  extraction  is  intended.  Individual  motion 
is  diagnostic  of  separate  teeth,  and  is  readily  induced,  when  the 
crowns  are  together,  by  pressing  a  strong,  thin,  flat-bladed  instru- 
ment between  the  teeth  and  turning  it.  The  teeth  are  seen  to  move 
apart. 

'  Private  communication. 


234  DENTITION 

The  pressure  of  an  erupting  third  molar  upon  the  second  molar 
may  cause  neuralgic  pains,  and  at  times  the  teeth  in  general,  as  far 
forward  as  the  central  incisor,  may  seem  to  loosen  up  and  become 
tender  to  touch  and  again  become  comfortable  and  tight.  These 
symptoms  may  be  repeated  apparently  in  consonance  with  the  efforts 
at  eruption.  This  pressure  also  causes  irregularities  of  alignment 
or  breaks  up  an  orthodontia.  Their  extraction  for  this  reason  is 
sometimes  indicated. 

Owing  to  insufficient  development  at  the  angle  of  the  jaw,  it  is 
almost  the  rule  that  the  eruption  of  the  lower  third  molar  is  attended 
with  some  degree  of  discomfort  due  to  gum  and  bone  irritation,  and, 
possibly,  to  pressure  on  the  formative  pulp  (Fig.  111). 

For  some  months  prior  to  eruption,  heavy,  gnawing,  rheumatic 
pains  may  be  indefinitely  located  about  the  jaw  and  ear  of  the 
affected  side.  The  muscles  of  mastication  become  stiff  and  may 
contract  spasmodically,  simulating  trismus.  These  symptoms,  if 
severe,  may  be  relieved  by  deep  X-incisions  in  the  gum;  or,  if  mild, 
by  the  application  of  non-discoloring  rubefacients  or  sedatives  to 
the  outside  of  the  face,  over  the  affected  parts.  The  massage  of  the 
parts  affords  some  relief.    Flagg  recommended  the  following: 

I^ — Tinct.  opii, 

Tinct.  aconiti, 

Chloroformi p.  seq. — M. 

Sig. — To  be  rubbed  on  the  outside  of  the  face. 

I^ — AconitiriEe gr.  j 

Cerati  simphcis Bj — M. 

Sig. — To  be  well  spatulated.  To  be  distended  with  oil  of  cloves  or  phenol 
camphor  and  gently  rubbed  on  the  outside  of  the  face,  the  mouth  and  eyes  to  be 
particularly  avoided. 

Or,  when  the  aconitine  fails  to  produce  relief: 

ly — Veratrinse gr.  xx 

Cerati  simplicis §j — M. 

Sig. — To  be  used  in  the  sanre  manner  as  the  aconitine. 

As  the  tooth  advances,  the  symptoms  may  become  progressively 
severe.  The  gum  may  become  inflamed,  swollen,  and  be  masticated 
upon,  the  oral  pyogenic  organisms  produce  infection,  presumably 
finding  an  entrance  at  the  point  proximating  the  second  molar.  The 
patient  suffers  from  the  pain  and  inability  to  masticate  and  swallow, 
and  becomes  nervous,  irritable,  and  debilitated;  the  breath  becomes 
fetid  and  the  salivation  excessive.  The  inflammation  extends  into 
the  contiguous  tissues,  and  pus  may  form,  extending  into  them; 
swelling  may  occur  in  the  adjacent  glands,  parotid,  submaxillary,  etc. 


THE  SECOND  DENTITION  .  235 

It  may  also  extend  to  the  tonsil  or  pharynx.  All  mastication  is  pre- 
vented, fever  is  present,  and  the  patient  prostrated;  septicemia  and 
death  may  follow.^  Reflex  pains  may  occur.  Brown^  relates  a  case 
of  noma  which  developed  from  an  infection  in  this  location.  The 
gangrenous  condition  extended  to  the  lungs.      Death  ensued. 

Results  similar  to  these  may  occur  when  the  crown  is  partly 
erupted,  being  covered  at  its  distal  portion  by  a  curtain  of  gum 
which  may  be  ulcerated  upon  its  under  surface.  This  curtain  of 
gum  may  be  thin  and  stretched,  or  project  rather  rigidly  over  the 
tooth  without  stretching,  as  though  attached  to  it. 

In  these  latter  cases  the  pus,  as  a  rule,  finds  egress,  but  occasionally 
it  burrows  into  the  pocket  between  the  tooth  and  contiguous  tissue, 
causing  much  inflammation  or  pus  formation.  When  gum  pockets 
remain  about  teeth,  food  may  ferment  in  them  and  cause  deep  pus 
formations  which  may  result  in  Ludwig's  angina,  a  frequently  fatal 
disease.    (See  Ludwig's  Angina.) 

Treatment. — The  treatment  depends  upon  the  stage  to  which  the 
inflammation  has  advanced. 

If  the  patient  be  able  to  partly  open  the  mouth,  the  part  may  be 
sterilized  by  spraying  it  with  a  germicide  such  as  a  1  to  2000  solution 
of  mercuric  chloride  in  hydrogen  dioxid  [or  hot  carbolized  water, 
followed  by  application  of  tincture  of  iodin.  (Brown.)]  Following 
this  an  injection  of  novocain  solution  is  made  into  the  flap  of  tissue, 
and  the  gum  completely  removed  from  over  the  face  of  the  crown, 
or,  if  feasible,  any  pocket  wall  cut  away. 

To  accomplish  this,  a  deep  linear  cut  is  made  with  a  sharp  bistoury, 
extending  from  the  distolingual  to  the  mesolingual  angle  of  the 
crown.  A  similar  cut  is  made  from  the  distobuccal  to  the  meso- 
buccal  angle.  If  not  already  free,  the  gum  is  divided  at  its  mesial 
contact  with  the  distal  surface  of  the  second  molar.  The  block  is 
now  penetrated  by  a  tenaculum,  drawn  tense,  and  the  final  cut  made 
at  the  distal  border  with  decidedly  curved  gum  scissors.  Less 
cutting  is  required  in  some  cases.  A  special  gum  guillotine  is 
obtainable,  which  practically  bites  out  a  piece  of  the  gum  flap.  The 
electric  cautery  may  be  used  to  burn  away  the  gum  tissue  (Fig.  175). 

The  hydrogen  dioxid  spray  should  be  again  applied  to  remove  any 
possible  pus  germs  present,  and  should  be  repeated  at  intervals  of 
about  two  hours.  Tincture  of  iodin,  diluted  about  one-half  with 
alcohol,  may  be  applied  every  few  hours,  by  means  of  cotton  wound 
on  an  applicator  or  tooth  pick,  and  exerts  a  germicidal  effect.  A 
neglect  of  this  simple  precaution  gave  the  editor  a  week  of  personal 

1  Flagg,  and  occasional  reports.  2  Dental  Cosmos,  1908,  p.  5. 


236  DENTITION 

discomfort  and  inability  to  masticate,  after  the  removal  of  a  trifling 
and  apparently  non-inflamed  flap  of  gum.  A  cold  compress  should 
be  recommended  for  the  angle  of  the  jaw,  if  deemed  advisable. 
Magnesium  sulphate  as  a  derivative  may  be  used  with  advantage. 

Fig.  175 


Ash's  gum  guillotine. 

If  the  patient  be  confined  to  his  bed  and  unable  to  open  the  jaws, 
a  more  difficult  operation  presents.  The  first  object  should  be  to 
reduce  the  intensity  of  the  inflammatory  symptoms.  This  is  accom- 
plished by  the  removal  of  the  gum  block  as  above,  if  the  mouth  can 
be  opened  sufficiently.  Anesthesia  may  be  resorted  to,  after  oral 
sterilization,  for  the  purpose.     A  jaw  separator  is  introduced,  and 

Fig.  176 


Gum  scissors. 

operated  until  sufficient  space  is  gained  and  the  cuts  made.  If  no 
more  be  possible  at  the  first  visit,  the  lingual  and  buccal  linear  cuts 
should  be  made  to  insure  free  bloodletting,  which  may  be  increased 
by  syringing  forcibly  with  lukewarm  water,  the  position  of  the 
patient  being  such  that  gravity  favors  its  flowing  out  of  the  mouth. 
Cold  compresses  are  to  be  placed  over  the  angle  of  the  jaw  and 
magnesium  sulphate  and  the  hot  pediluvium  administered  as  deriva- 


THE  SECOND  DENTITION  237 

tives.  Cataplasma  kaolini,  a  compound  of  kaolin  (Chinese  clay), 
boric  acid,  methyl  salicylate,  glycerin,  and  small  quantities  of  thymol 
and  oil  of  peppermint,^  are  useful,  applied  in  quantity  to  the  face, 
externally.    The  antiseptic  sprays  are  to  be  used  as  before  directed. 

If,  in  addition,  local  massage  or  electric  heat  and  massage  over  the 
angle  of  the  jaw  be  practised,  the  swelling  and  muscular  hardness 
usually  disappear  in  a  few  days.  It  is  well  to  then  remove  the 
entire  block  of  gum  to  prevent  reinfection.  There  can  be  no  ques- 
tion that  complete  anesthesia  and  thorough  gum  block  removal,  at 
the  first  visit,  is  the  most  advisable  surgery.  (See  Apical  Abscess, 
third  stage.) 

If  the  third  molar  be  correctly  placed,  its  eruption,  as  a  rule, 
proceeds  uninterruptedly  from  this  point,  though  it  may  never  be 
entirely  free  from  some  degree  of  overlapping  b.y  the  gum  tissue, 
owing  to  arrest  of  eruption  by  the  occlusion  of  the  more  advanced 
upper  third  molar.  Pockets  are  thus  formed  which  favor  food 
retention,  which,  undergoing  fermentation,  may  either  cause  ulcera- 
tion of  the  soft  parts,  or  caries  of  the  distal  and  distobuccal  surfaces 
of  the  tooth. 

Grinding  the  occlusal  face  of  the  upper  molar  may  assist  eruption  of 
the  lower.  The  gum  flap  should  be  anesthetized  and  removed  by  the 
thermocautery;  or  if  inflamed,  be  sprayed  with  hydrogen  dioxid,  and 
a  pellet  of  cotton  saturated  with  eugenol  introduced  for  a  short  time. 
More  marked  malposition  may  cause  difficulty  of  eruption, 
necessitating  the  extraction  of  the  third  molar  or  even  of  the  second 
molar.  In  some  cases  it  may  be  better  to  also  extract  the  upper 
third  molar,  as  it  will  probably  elongate  in  time  and  allow  food  to 
pack  into  the  interspace  mesial  to  it.  A  presentation  of  the  occlusal 
face  of  the  third  molar  to  the  distal  surface  of  the  second  molar  is  a 
common  form  of  malposition. 

If  very  deep  seated,  the  third  molar  may  at  times  be  diagnosticated 
in  this  position  by  passing  an  explorer  or  thin  right-angled  blade 
down  the  distal  surface  of  the  second  molar,  or  b}^  means  of  a  deep 
incision  with  a  bistoury  or  exploring  needle.  Failing  this,  or  prefer- 
ably, replacing  it,  the  .a--rays  are  a  very  valuable  means  of  diagnosis. 
In  this  situation,  pathological  resorption  of  the  root  of  the  second 
molar  may  result,  and  irritation  of  its  pulp  be  added  as  a  compli- 
cation. In  this  case  the  second  molar  must  be  extracted.  (See 
Malposition.) 

A  more  common  form  of  presentation  exhibits  the  distal  surface 
of  the  crown  above  the  gum  and  the  meso-occlusal  angle  locked 

1  Antiphlogistin  is  the  proprietary  equivalent. 


238  DENTITION 

beneath  the  cervix  of  the  second  molar  (Fig.  174).  Caries  is  not  in- 
frequently induced  by  the  retention  of  food.  The  third  molar  may  be 
removed  by  an  operation  involving  the  surgical  removal  of  a  portion 
of  the  base  of  the  coronoid  process,  followed  by  extraction.  The  pulp 
of  the  third  molar  may  be  devitalized  by  arsenic  applied  and  sealed 
in  a  pitj  drilled  in  its  distal  surface.  After  death  of  a  portion  of  the 
pulp,  the  pit  may  be  made  to  perforate  the  crown  from  side  to  side, 
and  then  a  dentate  fissure  bur  mounted  in  the  right-angle  handpiece, 
or  a  disk,  may  be  used  to  saw  off  the  occlusal  half  of  the  crown.  In 
the  space  thus  gained,  and  between  the  second  and  third  molars,  a 
wedge  of  sea-tangle  may  be  neatly  fitted;  its  swelling  causes  mutual 
separation,  which  loosens  the  third  molar  somewhat,  by  the  process 
of  resorption.  It  should  now  be  quite  readily  extracted  by  appro- 
priate movements. 

Cryer  recommends  the  removal  of  the  occlusal  section  of  the 
crown  of  the  third  molar  by  means  of  a  carborundum  disk,  and  the 
removal  of  the  tooth  by  means  of  forceps  or  elevators.  Extraction 
in  such  a  case  must  be  carefully  done.  The  use  of  the  elevator  is 
dangerous,  unless  laterally  applied,  as  there  is  danger  of  fracture  of 
the  ramus,  which  has  occurred.    (Schamberg.) 

The  loss  of  a  second  molar  may  be  for  other  reasons  necessary, 
but  such  a  loss  in  the  last  case  described  is  equivalent  to  a  loss  of 
two  teeth,  as  the  third  molar  will  be  of  little  value. 


CHAPTER  VIII. 

MALFORMATIONS  AND  MALPOSITIONS  OF  THE 

TEETH. 

Abnormalities  of  the  teeth  are  found  associated  with  position, 
size,  form,  and  structure.  Aberrations  in  form,  structure,  and  size 
are  inchided  under  the  head  of  malformations  of  the  teeth;  aberra- 
tions of  position  are  discussed  under  the  head  of  malpositions  of  the 
teeth.  The  particular  section  of  dentistry  relating  to  malpositions 
of  the  teeth  is  by  general  consent  made  a  special  department  of 
operative  dentistry,  that  of  orthodontia;  but  many  of  the  phases 
of  the  subject  are  of  great  pathological  interest,  although  the  thera- 
peutic measures  usually  demanded  are  mechanical  in  character  and 
clearly  belong  to  the  fields  of  operative  and  prosthetic  dentistry. 

Malformations  of  the  teeth  may  be  macroscopic  or  visible  to  the 
naked  eye,  or  microscopic,  requiring  special  preparation  for  obser- 
vation under  the  microscope. 

The  causes  of  imperfectly  formed  enamel  or  teeth  must  be  sought 
by  study  of  the  conditions  preceding  their  development.  That  modi- 
fications of  general  nutrition  must  modify  tooth  development  seems 
to  be  a  safe  proposition. 

An  ill-nourished  child  is  apt  to  have  at  least  poorly  organized  tooth 
material,  while  in  one  that  has  actually  undergone  an  exanthematous 
disease  the  tooth  form  subsequently  seen  is  frequently  found  to  have 
been  profoundly  modified  by  the  disease. 

MICROSCOPIC   MALFORMATIONS. 

Microscopic  or  histological  defects  of  the  teeth  may  affect  any  of 
the  dental  tissues,  enamel,  dentin,  cementum,  pulp,  or  pericementum. 

Enamel. — Defects  in  enamel  structures  range  from  any  degree  of 
orderliness  in  the  even  distribution  of  globular  bodies  and  cementing 
substance  in  the  tissue,  to  gross  aberrations  in  formation.  The  finer 
variations  of  structure  are  not  easily  recognizable. 

Theoretically  perfect  enamel  should  show  in  longitudinal  section  a 
series  of  squares  of  uniform  size  built  into  rods,  the  outlines  of 
the  squares  and  rods  being  marked  by  lines  of  cementing  substance 
having  a  refractive  index  slightly  different  from  that  of  the  squares 

( 239 ) 


240     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

(Fig.  118).  While  such  a  structure  is  perhaps  never  found,  it  is 
difficult  to  draw  a  line  where  aberrations  from  such  a  standard  become 
pathological.  An  arbitrary  standard  might  be  assumed  as  follows: 
Regard  any  enamel  as  pathological,  where  areas  of  it  differ  from  its 
general  substance  to  such  an  extent  as  to  have  a  decidedly  different 
refractive  index.  A  typical  form  of  abnormality  is  noted  in  what 
are  known  as  opaque  spots  in  the  enamel,  areas  in  which  an  opaque 
surface  exists  instead  of  the  normally  translucent  enamel. 

Fig.   177 


Portion  of  a  white  spot  in  enamel,  showing  lacli  of  interprismatic  cement  substance. 
X  2000.     Compare  with^Fig.  343.     (Williams.) 


Opaque  Spots  in  Enamel.— White,  brown,  and  corn-colored  opaque 
areas  of  enamel  are  frequently  seen,  surrounded  by  apparently  normal 
enamel. 

Examined  without  the  aid  of  the  microscope  they  are  seen  to 
present  a  surface  as  smooth  as  any  enamel,  though  sometimes  slightly 
crenated,  but  upon  this  surface  being  broken  up  with  a  bur  a  chalky, 
granular,  whitish  material  containing  at  times  the  yellowish  pigment 


MICROSCOPIC  MALFORMA TIONS 


241 


is  seen,  sometimes  occupying  the  entire  thickness  of  the  enamel. 
These  spots,  if  slight,  are  sometimes  without  this  granular  character, 
while  the  pigment  affects  the  entire  thickness  of  the  enamel. 

Williams  submitted  the  enamel  at  the  borders  of  such  spots  to 
microscopic  examination,  and  compared  it  with  enamel  in  the  first 
stages  of  decay,  finding  in  both  a  similar  appearance,  characteristic 
of  a  lack  of,  or  a  loss  of  interprismatic  cement  substance  (Fig.  177). 

Fig.   178 


Section  through  human  cuspid,  showing  sulcus  and  appearance  of  tissue  in  its  vicinity. 
X  75.     (Specimen  by  Choquet;  photograph  by  Williams.) 


Upon  the  data  derived  from  his  investigations  with  the  develop- 
ment of  the  enamel,  he  concluded  that  these  spots  are  due  to  a  lack 
of  such  cement  substance.  This  leaves,  as  the  probable  substance  in 
the  spot,  unfused  globules  mingled  with  some  pigment.  H.  A.  Flynn 
concludes  that  "as  about  87  per  cent,  of  children  born  and  raised  in 
Colorado  Springs  have  defects  in  enamel,  while  in  other,  close  by 
localities  these  are  moderately  found,  the  cause  must  lie  in  the  lack 
of  lime  in  vegetable  matters  in  that  locality  and  hence  in  the  milk 
of  cows  fed  upon  them.  This  lack  together  with  the  great  demand 
of  the  developing  osseous  system  for  lime  causes  a  deficiency  for 
the  relatively  non-important  teeth. "^    In  one  case  of  an  adult  lady,  a 


16 


'  Items  of  Interest,  January,  1910. 


242     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

broad,  brown  spot  was  seen  on  a  lower  left  lateral.     There  was  a 
history  of  the  temporary  lateral  having  been  knocked  out. 

Enamel  formation  about  the  sulci  of  teeth  is  frequently  faulty; 
owing  to  an  imperfect  union  of  the  enamel  segments  forming  the 

Fig.  179 


Section  of  human  molar,  showing  dentinal  fibrillse  penetrating  enamel.      X  600. 

(WiUiams.') 


cusps  of  the  teeth,  minute  fissures  exist  in  the  enamel;  these  are 
most  marked  in  the  fissures  of  molars,  as  shown  in  Fig.  178.  The 
enamel  bounding  these  fissures  has  an  irregular  structure. 

The  dentinal  fibrillse  may  penetrate  the  substance  of  the  enamel 
(Figs.  179  and  184),  occupying  defined  channels  in  its  substance; 

1  For  an  interesting  article  illustrating  this  point  see  Boedecker,  Dental  Cosmos, 
1911,  p.  1000. 


MICROSCOPIC  MALFORMATIONS  243 

this  was  formerly  regarded  as  a  developmental  accident.  Caush'^ 
claims  to  have  found  this  to  be  a  normal  condition  of  human  enamel, 
and  regards  these  as  nutrient  spaces.  Still  later  Boedecker  has 
found  them  to  frequently  occur  in  enamel  (Fig.  184).  Andrews^ 
states  that  '  examination  of  sections  at  the  junction  of  formed  dentin 
and  ameloblasts  show  fibres  span  any  space  formed  between  them.' 
Evidently  there  must  have  occurred  a  mixture  of  the  elements 
of    dentin    and    enamel,    the    record    showing    an    interdigitation 

Fig.   1^^0 


Section  of  human  incisor,  sliowing  "bands  of  Retzius"  and  marked  stratification  of 
enamel.     X  125.      (Williams.) 

of  papilla  (probably  odontoblasts)  and  enamel  organ  (probably 
ameloblasts).  After  calcification  these  odontoblastic  fibers  are 
caught  in  the  enamel.  Von  Beust  also  has  experimentally  shown 
this  (Fig.  109).  Such  conditions  are  not  to  be  confounded  with 
fissures  of  enamel  where  large  lines  of  faulty  calcification  or  non- 
calcification  extend  through  the  thickness  of  enamel.  A  portion 
of  the  enamel  may  occupy  an  area  within  the  dentin.    This  in  itself 

^  International   Dental  Journal,   June,    1904. 
2  Dental  Cosmos,  1912,  p.  49. 


244     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

shows  that  the  enamel  and  dentin  organs  can  be  heterogeneously 
arranged.    An  odontoma  is  another  evidence. 

Enamel,  even  normal  enamel,  is  not  of  uniform  composition;  were 
it  so,  it  would  exhibit,  in  addition  to  an  orderly  arrangement  of  its 
histological  elements,  a  uniformity  in  color.  So  common  are  differ- 
ences in  this  direction  that  the  presence  of  pigment  bands  must  be 
regarded  as  normal.  It  is  the  rule  to  find  enamel  traversed  by  deeply 
pigmented  parallel  bands,  which  pass  obliquely  upward  from  the 
surface  of  the  dentin  to  the  surface  of  the  enamel.  These  are  termed 
the  bands  of  Retzius;  they  appear  to  mark  the  size  of  the  enamel 
cap  at  successive  periods  of  its  growth  (Fig.  180). 

Fig.  181 


Section  of  enamel  from  syphilitic  tooth,  with  appearances  resembling  the  lacunae  of 
cementum.     X  600.    (Williams.) 


Stratification  and  striation  of  the  enamel,  as  shown  by  Williams, 
must  be  regarded  as  normal  physiological  records  of  the  mode  of 
enamel  formation.  Kirk  has  shown  that  normal  enamel  shows  vari- 
ations in  density  in  the  same  teeth. 

All  of  these  histological  defects  represent  variations  of  deposition, 
no  doubt  due  to  fluctuation  of  the  nutritive  processes  of  the  child  at 
the  time  of  tooth  formation.  Histological  records  made  in  the  enamel 
are  not  like  those  made  in  other  tissues,  for  there  is  no  certain  pro- 
vision through  which  such  defects  can  be  remedied  at  subsequent 
periods. 


MICROSCOPIC  MA  LFORMA  TIONS 


245 


l'rofoLUi(l  imtriti\'e  disturbances,  such  as  those  attending  hereditary 
syphiHs  in  children,  affect  the  structures  of  the  teeth.  One  of  the 
gross  results  of  this  disease  is  a  common  malformation  of  the  general 
form  of  the  incisors.  The  hard  tissues  of  such  teeth  exhibit  micro- 
scopic evidences  of  faulty  histology;  they  are  dull  and  opaque,  and 
traversed  by  irregular  bands.  Viewed  in  section,  the  enamel  of  such 
teeth  is  seen  to  be  almost  structureless  (Fig.  181).  Williams  found 
that  the  contents  of  the  large,  irregular  spaces  in  this  enamel  did  not 
respond  to  stains — i.  e.,  did  not  contain  organic  matter.  Such  teeth, 
when  not  presenting  gross  malformations,  may  have  a  distinct  irregu- 

FiG.  182 


4  -_ 


T 

/^^^ 

^ 

W 

j 

'^'^M 

J 

1 

^k 

' j^^^^^A 

\ 

f  ..^m 

1 

i 

B 

\ 

^^M 

1 

1 

^^■^n^Hv 

^'^^g 

% 

^ 

Enamel  and  dentin,  human  tooth:  1,  enamel;  2,  dentin;  1,  lines  of  Schreger  in 
enamel;  4,  brown  striae  of  Retzius.  (Probably  aggregation  of  tubes,  editor.)  (Bromell, 
after  Geise.) 


larity  of  enamel  surface.  This  may  even  be  seen  with  the  naked  eye, 
or  graphite  may  be  rubbed  over  the  teeth,  bringing  out  the  lines. 
Cloud-like  markings  are  also  seen  in  enamel,  which  are  called  the 
stripes  of  Schreger.  They  run  from  dentin  toward  the  peripher}-, 
and  are  considered  by  Pickerill  to  be  due  to  an  optical  effect  pro- 
duced by  superimposed  prisms^  (Figs.  182  and  183). 

There  is  evidence  that  other  forms  of  specific  dermatitis — scarlet 
fever  and  measles — which  occur  at  an  early  age  may  affect  the  for- 
mation of  enamel.     The  gross  defects  attributed  to  the  exanthemata 

1  Pickerill,  Dental  Cosmos,  October,  1913. 


246     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

are  irregular  pits  upon  the  crowns  of,  particularly,  the  incisors  (Figs. 
195,  etc.),  though  the  cuspids  and  first  molars  also  suffer.    In  some 

Fig.  183 


Lines  of  Schreger  in  the  enamel  of  a  permanent  and  deciduous  tooth  (human) . 
Bulge  of  enamel  at  cervix  of  deciduous  tooth  is  shown  due  to  bulging  of  dentin,  not 
to  thickness  of  enamel.     (Pickerill.) 

Fig.   184 


Specimen  of  decalcified  adult  enamel,  showing  enamel  prism  sheaths  and  lamella  (L), 
cut  longitudinally.     X  500.     (Boedecker.) 


MICROSCOPIC  MALFORMATIONS 


247 


cases  the  crowns  appear  honeycombed.  The  condition  is  known  as 
hypoplasia  of  the  enamel,  and  is  evidently  due  to  an  effect  upon  the 
enamel  organs.  The  microscopic  structure  is  also  affected.  There 
is  evidence  in  some  specimens  (Fig.  194)  that  the  dentin  may 
be  hypoplastic;  the  papilla  being  doubtless  affected  by  the  pre- 
vailing systemic  malnutrition.  The  dentin  being  first  developed, 
shows  perhaps  normal  for  a  distance,  then  a  row  of  interglobular 
spaces  is  found,  which  is  evidence  that  the  dentin  organ  is  affected 
by  the  general  disturbance  at  the  same  time  as  the  enamel  organ. 

Fig.  185 


Section  of  a  bicuspid  with  its  alveolus,  showing  a  pit-like  absorption  upon  the  side 
of  the  root  in  which  the  redeposit  of  the  cementum  has  begun:  a,  dentin;  b,  cementum; 
c,  peridental  membrane;  d,  bone  forming  the  wall  of  the  alveolus;  e,  absorbed  area  of 
cementum.  It  will  be  noticed  that  a  new  deposit  of  cementum  has  begun  the  filling 
of  the  area,  and  that  the  soft  tissue  in  the  area  of  absorption  is  of  a  cellular  type.  The 
bone  also  shows  the  effects  of  absorption  in  the  cutting  away  of  portions  of  the  ring 
of  the  Haversian  systems  at/,  while  at  g  the  presence  of  osteoclasts  shows  that  absorp- 
tion is  in  progress  at  that  point.     (Black.) 


Hopewell-Smith^  describes  the  enamel  developed  during  rickets  as 
faulty,  and,  in  so  far  as  limited  observation  could  determine,  con- 
tained numerous  spaces  probably  filled  with  soft  tissue.  These 
spaces  were  in  the  first-formed  portions  of  the  specimens  observed. 

Dentin. — Data  regarding  the  finer  phases  of  defective  histological 
structure  of  the  dentin  are  meagre.  It  has  been  observed  that  the 
dentinal  tubuli  of  some  teeth  are  much  larger  than  in  others  of  the 
same  age,  and,  no  doubt,  future  investigations  with  an  improved 
technique  directed  toward  a  study  of  the  exact  mode  of  dentin 
formation  will  exhibit  defects  more  certainly. 

The  chief  histological  defects  noted  in  dentin  are  areas  of  faulty 
or  non-calcification,  called  interglobular  spaces  (Fig.  186).     These 

1  Loc.  cit. 


248     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 


Fig.  186 


Section  showing  interglobular  spaces  in  dentin  of  a  syphilitic  human  tooth.    (Williams.) 

Fig.  187 


/ 


'"■■A, 


Interglobular  spaces  crossed  by  dentinal  tubes.    Prepared  by  Weil's  process.    Magnified 
240  times.    (Hopewell-Smith.) 


MICROSCOPIC  MALFORMATIONS  249 

are  most  common  in  tlic  dentin  immediately  underlying  its  co\'ering 
tissue;  so  common  in  the  dentin  under  the  cementum  that  this 
portion  of  dentin  has  been  called  the  stratum  grannlosum,  the 
granular  layer  of  Tomes  (Fig.  124).  In  the  })ody  of  the  dentin  these 
spaces  have  a  more  irregular  distribution. 

In  wet-ground  sections  (Hose)  the  dentinal  filaments  are  seen  to 
pursue  an  unbroken  course  through  these  areas.  The  contents  of  the 
interglobular  spaces  react  to  stains  like  the  sheaths  of  Neumann; 
that  is,  they  probably  contain  transitional  tissue.  These  areas 
probably  represent,  as  do  defective  spots  of  enamel,  periods  of 
depressed  vitality,  or  of  altered  nutrition.  In  the  light  of  present 
knowledge  regarding  the  subject,  they  are  to  be  viewed  as  areas  in 
which  the  calcific  process  was  faulty.  The  malformations  noted  in 
connection  with  the  enamel  of  teeth  have  their  analogues  in  the 
dentin  (Fig.  187;  also  Fig.  195). 

Fig.  188 


1 
1 


Schreger's  lines  in  dentin.     From  the  i\()r\'  of  the  tusk  of  a  walrus.     Prepared  by 
grinding.     Unstained.      X  45.       (Hopewell-Smith.) 

Interblobular  spaces  afford  some  evidence  of  the  formation  of 
dentin  by  a  deposition  of  globular  bodies  in  a  matrix  of  protoplasmic 
material.  The  continuation  of  the  tubules  through  the  mass  of 
uncalcified  contents  is  evidence  of  their  probable  independent  for- 
mation by  the  fibril  cells  (Fig.  187). 


250     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

Occasionally  lines  appear  in  dentin  at  a  common  developmental 
level  and  having  a  degree  of  parallelism  to  the  pulp  surface.  They 
are  evidently  records  of  a  new  period  of  increment  and  consist  of 
short  curves  in  the  tubules.  They  are  called  contour  lines  of  Owen, 
also  lines  of  Schreger,  in  dentin  (Figs.  188  and  189). 

Fig.  189 


The  same  as  Fig.  189.      X  420.     (Hopewell-Smith.) 

Histological  malformations  of  the  pulp  have  not  been  recorded,  the 
normal  histology  of  the  organ  not  being  made  out  with  sufficient 
certainty  to  determine  what  appearances  are  to  be  regarded  as 
abnormal.  Grosser  aberrations,  such  as  those  shown  in  Fig.  137, 
are  made  out. 

Cementum. — As  stated  in  Chapter  VI,  the  pericementum  con- 
tains numbers  of  multinucleated  cells — odontoclasts;  and  their 
presence  is  not  to  be  regarded  as  abnormal.  The  cementum  of  the 
roots  of  teeth  may  exhibit  evidences  of  former  action  of  these  cells 
in  excavations  of  cementum,  which,  by  a  subsequent  deposition  of 
cementum,  have  become  filled.  This  gives  an  irregular  course  to 
the  cement  laminae  (Fig.  185).  These  appearances  are  to  be  regarded 
as  not  necessarily  pathological,  for  the  following  reason:  for  some 
time  (years)  subsequent  to  the  eruption  of  the  teeth,  developmental 
changes  occur  in  the  alveolar  bones;  depositions  (subperiosteal) 
increasing  their  volume  are  accompanied  by  resorption  of  other 
portions  of  the  bone,  such  a  balance  being  kept  between  their  pro- 


MACROSCOPIC  MALFORMATIONS  251 

cesses  that  the  teeth,  although  shifting  their  positions,  are  kept  in 
normal  occlusion. 

The  cementum  may  be  thickened  by  additional  deposits,  as  in 
hypercementosis,  which  is  an  excess  of  development  classed  as 
pathological. 

MACROSCOPIC  MALFORMATIONS. 

The  teeth  may  vary  from  the  normal,  either  as  regards  size  or 
external  configuration. 

Variations  as  to  Size. — It  is  patent  to  the  most  casual  observer 
that  the  teeth  vary  as  to  size.  Comparisons  in  this  direction  are 
made  by  an  examination  of  the  upper  central  incisors.  Fig.  191 
shows  nearly  the  extremes  of  observable  sizes;  Guilford^  points  out 
that  excessively  large,  central  incisor  crowns  are  usually  supported 
by  abnormally  small  conical  roots.  Marked  giantism  of  the  central 
incisors  usually  occurs  in  pairs,  the  other  teeth  being  of  normal  size. 
On  the  other  hand,  dental  giantism  of  less  degree  may  involve  all 
of  the  teeth  of  a  denture.  The  molar  teeth  are  occasionally  of 
enormous  size,  the  bicuspids  rarely  so,  and  the  cuspids  next  in  fre- 
quency to  the  molars  as  to  the  occurrence  of  giantism.  Guilford 
observes  that  giantism  of  the  cuspid  crowns,  unlike  that  of  the 
central  incisors,  is  usually  accompanied  by  an  increased  size  of  root. 
He  mentions  the  case  of  a  cuspid  measuring  an  inch  and  one-half 
in  length  from  tip  to  tip. 

Fig.   190  Fig.  191 


Dwarf  Teeth. — Deficiency  in  size  is  of  more  common  occurrence 
than  excessive  size.  It  appears  to  occur  more  frequently'  with  the 
upper  third  molars  and  upper  lateral  incisors  than  with  any  other 
teeth.  Fig.  192  shows  the  extremes  in  size  between  two  perfectly 
formed  lower  third  molars.  The  stunting  of  these  and  of  other  teeth 
is,  however,  usually  associated  with  such  an  aberration  of  outward 
form  that  most  dwarf  teeth  must  be  considered  as  abnormal  in  form 
as  well  as  in  size.  The  writer  has  seen  a  supernumerary  with  crown 
and  root  together  measuring  one-eighth  inch. 

'  American  System  of  Dentistry,  vol.  iii. 


252     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

Fig.   192 


X'S'^ 


Tusk-like  permanent  central  incisors;  temporary  teeth  retained  on  either  side.     Female, 
aged  twenty- five  years. 


Fig.  193 


Conical  lateral  incisor  transformed  by  porcelain  crown. 


Fig.  194 


Hypoplasia  of  enamel,  showing  arrested  stratification;  dentine  shows  effects  of  hypo- 
plasia at  interglobular  spaces    (Hopewell-Smith.) 


MACROSCOPIC  MALFORMATIONS  253 

A  central  incisor,  or  more  frequently  a  lateral  incisor,  may  have 
a  conical  crown,  as  shown  in  Fig.  193.    The  condition  may  be  double. 

Upper  third  molars  frequently  consist  of  but  a  single  cone,  diminu- 
tive in  size;  at  times  a  crater-like  crown  is  formed  by  a  series  of  small 
cones  about  a  central  pit. 

Treatment. — The  Land  jacket  crown  is  very  useful  in  modifying 
the  cone  into  a  typical  tooth  form  (Fig.  193). 

Hypoplasia  of  the  Dental  Structures. — By  hypoplasia  in  this  con- 
nection is  meant  an  arrested  development  of  any  portion  of  a  tooth. 
Necessarily  the  tooth  is  deformed. 

Fig.  195  Fig.   196 


Hypoplasia  due  to  eruptive  fevers.  Hypoplasia  of  incisal  portion  of  enamel. 

The  term  atrophy  has  been  used  in  this  sense,  but  is  better  confined 
to  a  lessening  in  size  after  normal  development  of  a  part  has  occurred. 
(See  p.  79.)  Nutritional  disturbances,  the  exanthemata,  and  syphilis 
all  seem  to  have  a  profound  influence  upon  the  form  of  teeth  develop- 
ing during  the  period  of  active  disease,  by  affecting  the  cells  of 
the  formative  organs.  With  the  passing  of  this  period,  the  develop- 
ment of  the  tooth  may  proceed  in  an  orderly  manner.  The  fol- 
lowing forms  of  hypoplasia  are  known : 

Pitted  and  Grooved  Teeth. — The  hypoplasias  described  under  this 
heading  may  consist  of  a  series  of  irregular  grooves  or  pittings,  the 
crowns  having  approximately  the  normal  outlines.  Of  these  malfor- 
mations Figs.  197  to  200  are  fairly  typical. 

Black  regards  the  formation  of  pits,  the  simultaneously  developed 
zone  of  enamel  being  perfect,  as  due  to  aberration  in  development  of 
enamel  rods,  leaving  a  hole  (doubtless  a  localized  effect  upon  the 
ameloblasts) .  Histologically  the  strata  of  the  enamel  partly  fail  of 
deposition  at  these  points  (Fig.  195). 

With  a  history  of  a  case,  including  the  age  of  the  child  at  the  period 
of  the  disease,  if  examination  be  made  of  the  positions  of  the  defects, 
the  age  will  serve  as  an  indication  as  to  whether  there  has  been  any 
connection  between  the  eruptive  fever  and  the  dental  malformation. 
For  example,  if  enamel  pits  upon  incisors  have  been  caused  by  an 
eruptive  fever  between  the  ages  of  four  and  five,  they  should  occupy 


254     MALFORMATIOXS  AXD  MALPOSITIOXS  OF  THE  TEETH 

a  part  a  little  above  the  half-way  area  of  the  crown  face  of  a  central 
incisor.  The  lateral  will  be  affected  nearer  the  incisal  edge  and  the 
cuspid  still  more  so;  it  is  ex-ident  that  the  enamel  being  already 
formed  about  the  incisal  edge  of  the  tooth,  alterations  of  nutrition 
could  not  affect  the  already  formed  tissue.  (See  Fig.  116.)  The 
enamel  formed  after  a  period  of  attack  may  be  perfect  (Figs.  197  and 
200). 

Fig.  197  Fig.  198 


Showing  the  front  teeth  grooved  from  the  alternation  of  perfectly  and  imperfectly 
developed  portions  of  enamel.    Hypoplasia.    (Tomes.) 

Hutchinson's  Teeth  (Hypoplasia  . — During  the  first  few  weeks 
after  birth,  skm  eruptions  characteristic  of  hereditary  s^'philis  are 
apt  to  occur  in  the  contaminated  child.  At  this  period  the  tips  of 
the  permanent  incisors  are  undergoing  development,  the  first  per- 
manent molar  having  started  at  the  twenty-fifth  week  of  gestation 
(see  Fig.  116),  and  the  effect  of  the  s\-philitic  eruption,  during  which 

Fig.  199 


Malformations  of  incisal  half  of  crowns,   with  cervical  half  jjerfect. 
(Model  by  W.  A,  Capon.) 


Hypoplasia. 


the  protozoon  treponema  pallidum  may  be  in  the  enamel  organ  (or 
there  is  a  severe  disturbance  of  metabolism  brought  about  by  the 
infection,  according  to  the  preferred  view  of  SteinO,  is  to  cause 
a  disturbance  of  the  enamel  organ  and  papilla,  which  produces  a 


»  Dental  Cosmos,  July,  1913,  p.  69-3. 


MArROSCOPIC   MALFORMATIONS  255 

defective  development  at  this  point.     Instead  of  the  normal  angles 
and  flattened  curves  of  the  labial  surfaces,  the  incisors  may  have 

Fig.  200 


Pitted  and  fringed  teeth,  some  of  them  carious  at  the  incisal  edges.    Specimen  in 
museum  of  Philadelphia  Dental  College. 


Fig.  201 


Hutchinson's  teeth.  Hypoplasia.  Two  upper  centrals  notched  and  contracted. 
Characteristically  undeveloped  upper  jaw.  From  an  hereditarj-  sj-phiHtic,  aged 
twelve  years. 

a  roughly  rounded  and  stunted  appearance.  The  incisal  edge  of 
the  tooth  is  narrower  than  its  neck.  The  enamel  at  this  edge  is 
irregularly  and  badly  formed;  but  there  is  a  semblance  of  the  three 


256     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

enamel  tubercles  found  normally.  The  middle  tubercle,  being  com- 
posed of  defective  enamel,  is  soon  lost  by  abrasion,  causing  the 
tooth  to  have  a  notched  appearance  (Figs.  201,  202,  and  203).  Stein 
quotes  an  old  authority  as  having  seen  one  central  notched 
and  the  other  normal.  The  first  permanent  molars  are  often 
exceedingly  corrugated  and  pitted,  the  pits  extending  into  the 
dentin.  These  pits  often  decay,  the  points  are  broken  or  worn  away, 
sometimes  leaving  a  discolored,  often  black  surface.     (Fig.  204.) 

In  an  exhaustive  treatise  upon  this  subject,  Cavallaro^  has  shown 
that  the  pitted  cuspal  deformity  of  the  first  molars,  the  notched 
incisors  of  Hutchinson,  and  the  dystrophic  cusps  of  canines  in  the 
permanent  set,  as  well  as  similar  effects  occurring  in  the  temporary 
set,  are  the  stigmata  of  hereditary  syphilis,  either  direct  or  in  the 
second  generation.  He  found  the  treponema  pallidum  in  the  dental 
follicles  of  syphilitic  fetuses. 

Fig.  202  Fig.  203 


-^.  --.\ 


Syphilitic  teeth  in  upper  and  lower  jaws  The  teeth  of  hereditary  syphilis  at 

as  they  appear  when  recently  erupted.  maturity. 

He  calls  attention  to  the  possible  effect  upon  the  first  molar  enamel 
(developing  before  birth)  alone,  as  indicating  the  cessation  of  tre- 
ponemal activity,  though  the  incisor  enamel  (developing  after  birth) 
is  usually  affected.  The  cuspid  (developing  still  later)  may  not  be 
affected;  which  shows  a  cessation  of  germ  activity  between  incisor 
and  cuspid  development.  The  dental  stigmata  may  thus  occur  in 
the  absence  of  the  under-developed  body  and  other  physical  charac- 
teristics of  syphilis,  though  these  may  also  be  in  evidence,  as  well  as  a 
history  or  eyidence  of  more  or  less  active  manifestations  of  syphilis.^ 

1  Dental  Cosmos,  1908. 

2  No  matter  what  conviction  a  dentist  has  that  these  dystrophies  are  of  syphilitic 
origin,  he  must  be  cautious  regarding  the  expression  of  his  opinion.  Even  the  thought- 
less leaving  of  a  cop5^  of  this  volume  upon  the  desk  from  which  it  was  picked  up  and 
this  chapter  seen  by  a  lady  patient,  produced  questions  of  a  very  embarrassing  character, 
regarding  certain  defects  in  her  child's  teeth.  Unfortunately,  Cavallaro's  investi- 
gations do  not  take  sufficient  cognizance  of  the  possible  intervention  of  other  exanthe- 
mata, either  in  the  subject  or  mother;  for  example,  in  his  Case  XX,  a  girl,  aged  four- 
teen years,  hereditary  syphilitic  showing  transverse  grooves  in  the  teeth,  the  effects 
are  attributed  to  syphilis.  The  child  may  easily  have  had  other  complications,  such 
as  measles.  Stein  excludes  rachitis,  variola,  scarlatina,  diphtheria,  typhoid  and 
rheumatism  as  very  rare  possible  causes  of  the  hypoplasia. 


MACROSCOPIC  MALFORMATIONS 


257 


Stein^  argues  that  as  the  stigmata  are  bilateral  and  symmetrical, 
they  could  not  have  been  produced  by  causes  acting  locally,  but 
that  the  general  disturbance  of  metabolism  affecting  the  develop- 
mental organs  of  the  teeth  causes  interference  with  the  functions 
of  such  of  them  as  should  be  actively  developing  tooth  structure. 

Fig.  204 


Semidiagrammatic  representation  of  a  systematized  hypoplasia  of  several  kinds  of 
upper  and  lower  teeth.  The  general  systemic  disturbance  which  must  have  caused 
these  stigmata,  commenced  about  the  twenty-fifth  week  of  intra-uterine  life  and  con- 
tiiiued  up  to  about  the  fourth  month  after  birth.  (The  third  molars  omitted.) 
(Stein.) 


While  to  syphilis,  may  now  be  accredited  much  of  the  pittings  upon 
teeth,  the  history  of  an  attack  of  one  of  the  exanthemata,  such  as 
scarlet  fever  or  measles,  at  a  certain  age  corresponding  to  the  devel- 
opment of  the  particular  part  of  the  tooth  which  has  undergone 
hyperplasia  makes  it  rational  to  accredit  the  effect  to  such  exanthema. 
Measles  often  causes  characteristic  eruptions  in  the  mucous  mem- 
brane of  the  mouth  and  pharynx,  and  could  easily  affect  the  dental 
follicle.  If  the  disease  and  the  effect  do  not  correspond  chronologic- 
ally they  should  not  be  related.  Syphilis  is  in  a  way,  an  exanthem- 
atous  disease  of  chronic  nature. 

In  hereditary  syphilitics,  Cavallaro  found  the  following  dental 
stigmata:  Hypoplastic  defects  of  systematic  character  with  predi- 
lection for  the  central  incisor  forming  the  notched  incisor  or  Hutchin- 
son's tooth,  and  also  cuspal  defects,  white  sulci,  white  marks,  delay 


17 


1  Dental  Cosmos,  July,  1913,  p.  695. 


258     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

of  development  and  eruption,  dental  infantilism,  microdontism, 
amorphism,  persistence  of  deciduous  teeth,  cuspal  defects  of  decidu- 
ous teeth,  especially  the  second  molar,  anomalies  of  structure, 
shape,  number,  direction,  arrangement,  and  color,  vulnerability  of 
the  dental  system,  ectopia,  total  or  partial  absence  of  teeth,  wearing 
away,  premature  caries,  premature  loss  of  teeth,  space  between  teeth, 
diastema.  Also  the  following  maxillary  stigmata:  malocclusion, 
defective  articulation  of  the  dental  arches,  prognathism,  ogival 
palate  and  cleft  palate. 

Fig.   205 


Hutchinson's  teeth,  cuspal  atrophy  of  canines  and  molars.     Multiple  sulciform  erosions. 

Diastema.      (Cavallaro.) 

Stein  offers  the  following  perhaps  more  clearly  expressed  classi- 
fication : 

"1.  Multiple  disseminated  stigmata  of  the  teeth,  both  in  the 
maxilla   and   the   mandible. 

2.  Symmetrical  stigmata  here- and  there  upon  homologous  teeth. 

3.  Systematized  stigmata  at  the  same  level  on  teeth  of  the  same 
kind,  but  at  a  different  level  on  different  kinds  of  teeth. 

The  most  characteristic  stigmata  of  the  teeth  of  heredosyphilis 
are: 

1.  Hypoplasia  of  the  four  first  molars. 

2.  A  systematized  hypoplasia  upon  the  several  upper  and  lower 
teeth. 

3.  Hutchinson's  teeth.  Microdontism  and  non-replacement  of 
deciduous  teeth  due  to  arrested  development  of  the  permanent 
successors  are  regarded  by  Stein  as  stigmata." 

Black^  states  that  any  malnutrition,  even  a  burn,  typhoid  fever, 
a  spasm,  etc.,  may  mark  teeth  as  a  nail  may  be  grooved.  He  claims 
to  have  seen  Hutchinson's^  teeth  without  history  of  taint. 

1  Dental  Review,  1906.  2  Dental  Digest,  1904. 


MACROSCOPIC  MALFORMATIONS  259 

As  it  ordinarily  causes  embarrassment  to  question  dental  patients 
regarding  syphillis,  the  Wassermann  and  luetin  reactions  may  be 
resorted  to  if  a  diagnosis  be  needed. 

Stein  states  that  the  Wassermann  may  be  positive  or  negative 
in  heredosyphilis. 

The  point  at  which  the  arrested  development  would  occur,  is  that 
part  under  development  at  the  time  the  nutritional  or  infective  dis- 
turbance occurs.  When  several  developing  teeth  are  attacked,  the 
centrals  are  marked  nearer  the  neck  than  laterals,  and  these  nearer 
than  cuspids.  The  first  molars  are  often  occlusally  defective,  as  well 
as  incisors,  and  sometimes  the  incisors  have  only  white  or  brown 
spots  instead  of  the  incisal  notch;  bicuspids  are  only  rarely  marked. 

A  lack  of  development  of  the  anterior  portion  of  the  upper  jaw 
has  been  noted  in  a  number  of  cases  clearly  syphihtic  (Fig.  201). 
It  has  been  noted  that  not  all  syphilitic  children  present  these  dental 
appearances;  and,  again,  appearances  said  to  be  identical  with  them 
are  observed  in  children  said  not  to  be  syphilitic;  nevei'theless,  the 
presence  of  such  teeth  is  usually  regarded  as  a  valuable  diagnostic 
sign  of  hereditary  syphilis.  The  existence  of  interstitial  keratitis 
and  of  chronic  catarrh  of  the  middle  ear,  in  connection  with  Hutchin- 
son's teeth  are  held  to  be  positively  diagnostic  signs  of  hereditary 
syphilis  (Hare). 

Oberwarth,^  in  a  synopsis  of  associate  symptoms,  mentions 
central  deafness,  chronic  hydrarthrosis  of  the  knee,  periostitis  of 
the  tibia,  tumefaction  of  the  spleen  and  liver,  radiating  cicatrices  of 
the  lips,  adenopathies,  ozena,  and  deformities  of  the  bridge  of  the 
nose,  cutaneous  gummata,  hemoglobinuria,  and  cerebral  phenomena 
as  possibilities  deduced  from  a  study  of  his  known  cases  of  hereditary 
syphilis. 

In  605  hereditary  syphilitics  observed  by  Sidler,  Huguenin,  and  the 
Fourniers,  the  stigmata  averaged  as  follows:  ocular,  50  per  cent.; 
dental,  43  per  cent.;  aural,  16  per  cent.^ 

Therapeutics  based  upon  such  a  diagnosis  are  followed  by  better 
results,  as  a  rule,  than  when  the  general  indication  is  ignored.  The 
boy  from  whose  mouth  a  model  (Fig.  201)  was  obtained,  had  inter- 
stitial keratitis  in  the  left  eye,  chronic  nasal  catarrh,  and  a  somewhat 
flat  development  of  the  nasal  bones. 

Tomes  favors,  and  adduces  evidence  to  support  the  contention  of 
Hutchinson,  that  honeycombed  incisal  edges  of  incisors  and  cuspids 
and  occlusal  surfaces  of  first  molars  are  indicative  of  mercurials 
administered  in  early  childhood. 

1  Review  by  Dental  Cosmos,  1908,  p.  179.         ^  Cavallaro:  Dental  Cosmos,  1909. 


260      MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

Pitted,  grooved,  or  otherwise  malformed  teeth  may  decay  some- 
times so  badly  as  to  produce  a  black,  slimy  appearance  almost 
loathsome  to  view.    In  other  cases  surprisingly  little  caries  develops. 

Agenesia  of  Enamel. — Cases  are  observed  where  there  has  been  a 
formative  crisis  to  the  extent  of  having  apparently  no  enamel  what- 
ever formed  over  the  occlusal  section  of  the  crown,  its  deposit  on 
the  remainder  of  the  crown  being  quite  normal  (Fig.  196). 

Fig.  206 


Dentinal  tubuli  terminating  in  the  spaces  of  the  granular  layer.    (Tomes.)- 

D.  B.  Freeman^  records  the  case  of  an  individual,  aged  twenty-six 
years,  whose  teeth  anterior  to  the  second  molar  were  entirely  devoid 
of  enamel.  The  condition  was  hereditary;  it  appeared  in  both 
brothers  and  sisters,  and  could  be  traced  back  for  three  generations. 

Hopewell-Smith^  claims  that  teeth  apparently  devoid  of  enamel 
have,  in  all  cases  examined  by  him,  had  attenuated  enamel  upon 
them.    This  would  also  be  classified  as  hypoplasia. 

Black^  has  described  the  teeth  of  a  man,  aged  twenty-seven  years, 
as  having  enamel  of  an  opaque,  paper-white  appearance,  as  readily 
cut  as  a  slate  pencil,  and  with  dentin  of  ordinary  consistence.  The 
teeth  presented  little  caries.  He  also  described  the  temporary  teeth 
of  a  child  as  all  without  trace  of  enamel,  the  dentin  soft,  bendable 
in  any  direction,  with  production  of  pain,  and  penetrable  with  a 
sharp  explorer  (agenesia  of  enamel). 

Treatment. — If  slightly  pitted,  gold  or  porcelain  fillings  may  be 
introduced.  Single  pits  collect  stains  which  are  not  removed  by  the 
brush.  It  is  well  to  concave  these  with  a  small  finishing  bur,  and  to 
furnish  the  patient  a  sharply  pointed  stick,  for  cleansing  with  tooth 
powder  or  pumice.  In  some  cases,  grinding  off  the  rough  incisal 
edge  is  sufficient;  in  other  cases  the  teeth  may  require  to  be  drawn 
down  after  this  procedure,  or  porcelain  inlays  may  be  used  to  restore 
the  incisal  edges.    In  the  extremely  disagreeable  cases  above  men- 

1  Guilford:  American  System  of  Dentistry,  vol.  iii. 

2  Histology  and  Patho.  Histology  of  the  Teeth. 
2  Dental  Cosmos,  June,  1908. 


MACROSCOPIC  MALFORMATIONS 


261 


tioned,  some  form  of  crowning  must  be  resorted  to.    Fig.  207  exhibits 
a  restoration  of  the  case  shown  in  Fig.  199. 

Hopewell  Smith^  has  observed  an  entire  absence  of  crowns,  not 
due  to  wear  or  caries,  both  on  upper  and  lower  teeth,  in  four 
generations  in  one  family.  Therefore,  they  are  cases  of  extreme 
hereditary  agenesia  of  the  crowns. 

Fig.  207 


Same  as  Fig.  178,  with  Land  jacket  crowns  placed  over  anterior  teeth.    (W.  A.  Capon.) 

Fusion  of  Teeth.^Two  or  more  teeth  may  be  united  during  the 
process  of  development.  The  union  may  occur  (1)  by  the  crowns, 
(2)  by  the  roots  alone,  and  (3)  by  both  crowns  and  roots. 

1.  Fused  teeth  united  by  the  crowns  alone  have  not  been  shown. 
The  nearest  approach  to  it  is  the  case  illustrated  by  Tomes,  in  which 
two  central  incisors  have  fused  by  union  of  the  crown  portions  and 
one-fifth  of  the  root  portions  of  the  two  teeth  (Fig.  208).  Such 
teeth  would  have  dentin  common  to  both  crowns  at  the  point  of 
union,  the  enamel  being  reflected  over  the  outside  of  the  common 
dentinal  mass,  according  to  the  scheme  shown  in  the  diagram  Fig. 
213,  B.  The  pulp  may  be  common  to  the  two  teeth  in  the  crown. 
Of  course,  the  root  pulps  are  separate. 

The  condition  is  a  record  of  the  fact  that  prior  to  dentification  the 
papillae  and  enamel  organs  of  the  two  teeth  have  coalesced  at  some 
point.  This  must  have  occurred  at  an  early  period,  perhaps  even 
during  the  descent  of  the  cords  into  the  jaw.  When  it  is  considered 
that  the  two  central  incisors  are  contained  in  two  separate  inter- 
maxillary bones,  the  rarity  of  such  a  union  and  in  such  a  manner 
may  be  appreciated.  I  have  seen  such  a  union  between  a  right  lower 
central  and  lateral  incisor,  in  the  mouth.  Recession  of  the  gum 
permitted  a  view  of  the  cervical  conformation. 


1  Dental  Cosmos,  August,  1913,  p.  781. 


262     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

2.  Those  teeth  united  by  fusion  of  the  roots  have  a  common  dentin 
at  the  point  of  union,  with  cementum  reflected  o^'er  that.  The  pulp 
is  common  to  the  two  teeth  at  the  point  of  fusion. 


Fig.  208 


Fig.  209 


Lingual  view.  Labial  view. 

Fusion  of  two  permanent  upper  central  incisors  by  their  crowns  and  a  portion  of  the 

roots.     (Tomes.) 

In  the  specimen  shown  in  Fig.  210  at  a  there  is  but  one  apical 
foramen.  In  that  shown  at  h  and  c  there  is  but  one  foramen  for  the 
two  fused  portions  of  pulp,  though  the  other  canals  have  their  usual 
foramina.  These  cases  evidence  an  accidental  coalescence  of  pulps 
after  much  independent  root  formation. 

Fig.  210 


a  b  c  d  e 

a,  fusion  of  two  molars  at  the  roots — two  pulp  cavities,  one  foramen;  b,  c,  fusion  of 
supernumerary  teeth  roofs  to  buccal  roots  of  upper  molars,  pulp  canal  conmion  where 
probes  cross;  d,  view  of  resorbed  root  end  of  two  fused  temporary  teeth;  e,  concres- 
cence by  hypercementosis. 


3.  Fusion  throughout  both  crowns  and  roots  have  the  same  charac- 
teristics as  the  others,  combined  in  the  one  specimen  (Fig.  214).  The 
diagram  (Fig.  213)  shows  the  scheme  for  the  crown  and  root. 

Fig.  216  shows  specimens  of  fusion  in  both  the  upper  and  lower 
jaws.     It  occurs  also  with  the  temporary  teeth   (Fig.  217).     Fig. 


MACROSCOPIC  MALFORMATIONS 


263 


213,  A  shows  a  very  rare  condition,  the  fusion  of  the  temporary 
central,  lateral,  and  cuspid  of  one  side  (triple  fusion). 


Fig.  211 


Fig.  212 


Attachment  of  temporary  teeth  by  their 
pericementi. 


Fusion  of  a  supernumerary  tooth,  with  an 
upper  third  molar. 


Fusion  is  evidently  an  abnormality  of  development,  dependent 
upon  coalescence  of  formative  organs  at  some  point,  and  is  most 
likely  to  occur  where  the  adjacent  tooth  follicles  have  least  anatomical 

separation  from  their  fellows.    The 
^  Fig.  213  ^  Foots  of  fuscd  temporary  teeth  are 

resorbed  as  usual  (Fig.  210,  d). 
No  particular   treatment  is  re- 
;  \  \\\  1  ^^y^'ii^       quired   unless  the  mass  in   some 

I     1^  \  ^^    ^^^\       way  causes  interference  with  func- 

FiG.  214 


A,  diagram  of  a  case  of  triple  fusion, 
showing  crowns  with  independent  in- 
cisal  edges  and  pulps;  but  otherwise 
fused  into  one  crown  with  one  pulp; 
B,  transverse  section  of  same,  showing 
common  pulp  cavity  and  common  den- 
tin overlaid  by  enamel  (or  cementum). 
From  a  perfect  specimen  in  the  editor's 
collection.     (Enlarged.) 


Permanent  central  and  lateral  incisors  of 
the  upper  jaw,  united  throughout  the  whole 
length  of  the  teeth.      (Tomes.) 


pulp, 


no 


tion,   which   is  unusual.    The  teeth   having   a    common 
attempt  should  be  made  to  divide  them. 

Fusions  are  most  common  betw^een  the  anterior  teeth  of  each  set  and 
between  the  second  and  third,  or  third  and  fourth  (supernumerary), 
permanent  molars.  It  has  not  been  noted  in  bicuspids,  presumably 
because  these  teeth  lie  in  the  bifurcations  of  the  temporary  molars. 

Concresence  of  Teeth. — Concresence  of  teeth  is  their  union  after 
the  tooth  is  formed ;  it  is  evident,  therefore,  that  the  union  can  only 


264     MALFORMATIONS  AND  MALPOSITIONS  OF  THE   TEETH 

be  caused  by  fusion  of  cementum.     This  means  that  during  the 
formative  and  eruptive  period,  or  after  eruption,  the  bony  partition 

Fig.  215 


Geminous  upper  laterals  with  common  pulp.     Practice  of  Dr.  Varney  Barnes. 
(Skiagraph  by  E.  Ballard  Lodge.) 

between  the  teeth  disappears,  and  that  their  pericementi  become 
united,  receding  from  the  hne  of  compression  as  cementum  is 
deposited  between  and  joining  the  roots.  The  united  teeth  show 
evidences  of  hypercementosis  at  points  other  than  the  point  of  union 

Fig.  216 


eE!i«jKn»."Si5 , 


A,    usion  of  upper  geminous,  permanent  laterals;  B,  fusion  of  lower  right  permanent 
central  and  lateral  incisions. 


(Fig.  210,  e,  and  Fig.  218).    At  times  the  roots  of  the  same  tooth 
undergo  either  fusion  or  concrescence. 


MACROSCOPIC  MALFORMATIONS 


265 


During  the  eruption  of  the  third  molars,  particularly  the  upper, 
temporary  lack  of  space  for  the  eruption  of  the  crown  may  cause 
resorption  of  the  bone  covering  the  roots  of  the  second  molar,  and 
fusion  of  the  formative  pericementum  of  the  third  molar  with  that 
of  the  second  occurs;  a  deposition  of  cementum  then  binds  the  teeth 
together,  preventing  the  eruption  of  the  third  molar.  More  than 
two  teeth  may  be  thus  united.  The  lower  third  molar  rarely  pre- 
sents its  roots  to  those  of  the  second  molar;  the  contrary  presentation 
is  the  rule. 

FiCx.  217 


Fusion  orupper  temporary  teeth. 


Double  fusion  of  lower  temporary  lateral  and 
cuspid. 


In  at  least  one  case,  the  crown  of  the  upper  third  molar  was  partly 
erupted  when  concrescence  occurred.  Retained  in  this  situation, 
the  crown  decayed  away,  necessitating  extraction;  the  second  molar 
came  away  with  it  (see  p.  266).  The  condition  also  occurs  apart 
from  the  eruptive  process.  Excessive  hypercementosis  upon  the 
roots  of  individual  teeth  may  finally  result  in  their  union  (Fig.  210,  e). 

The  only  treatment  required  for  concrescence  is  that  indicated 
for  impaction  or  hypercementosis  (which  see). 

The  tough  fibrous  gum  tissue  or  pericementum  has  caused  two 
temporary  teeth  to  be  extracted  together  at  times  (Fig.  211). 

Pont  cites  a  case  of  attachment  of  a  lower  first  molar  distal  root 
to  the  mesial  root  of  the  second  molar  by  a  strong  fibrous  ligament, 
2  mm.  in  diameter,  and  causing  fracture  and  removal  with  the  first 
molar.  There  is  also  sometimes  a  firm  fibrous  pericemental  attach- 
ment between  a  tooth  and  the  alveolar  process  or  bone.  In  one 
case  a  portion  of  the  antral  floor  was  torn  out  with  the  apical  tissue. 


266     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 


FiCx.  219 


Fig.  219  illustrates  a  remarkable  case  of  combined  fusion, 
concrescence,  flexion,  and  hypercementosis.  In  this  case  two 
abnormal  third  molar  crowns  were  first  formed.  The  roots  were 
fused  during  de^'elopment,  though  individual  single-pulp  canals 
were  formed,  which  joined  to  form 
one  foramen.  The  lapped  condition 
of  the  roots  was  due  to  pulp  flexion 
previous  to  root  deposition.  The 
carious  second  molar  roots  all  became 
hypercementosed  and  probably  from 
non-occlusion.  As  the  fused  teeth 
erupted,  they  presented  one  root  to 
one  root  of  the  second  molar. 

The  junction  of  these   occurred  as 
the  result  of  formations  of  cementum 

Fig.  218 


Concrescence.    Third  upper  molar  imprisoned 
between  the  roots  of  the  second  molar. 


Case  of  fusion  of  two  abnormal 
molars  and  concrescence  with  the 
root  of  a  right  upper  second  molar 
(restored  for  illustration.)  Pulp 
canals  shown  in  outline.  Common 
apical  foramen  (enlarged.)  (From 
author's  collection.) 


(concrescence).  The  widely  open  crater-like  pit  in  each  crown  shows 
the  persistence  of  soft  tissue  (enamel  organ)  at  that  point,  or  a 
lack  of  enamel  development  there. 

Mechanical  Union  of  Teeth. — Teeth  upon  extraction  are  occasion- 
ally found  united  by  alveolar  bone  which  is  locked  between  the 
roots  of  the  two  or  more  teeth  and  prefers  to  fracture  elsewhere. 
Occasionally  a  sequestrum  contains  several  teeth  (Fig.  172). 

Gemination  of  Teeth  (Twin  Teeth). — This  term  has  been  used  by 
Tomes  in  the  sense  of  union  of  teeth,  but  it  is  perhaps  better  used 
to  designate  supplemental  teeth  of  the  same  class.  In  twin  teeth, 
the  enamel  organ  of  a  permanent  or  temporary  tooth  is  duplicated, 
in  all  probability,  two  buds  arising  from  the  cord  or  band,  as  the 
case  may  be. 

In  gemination,  one  of  the  teeth  formed  is,  of  course,  a  supernu- 
merary tooth,  but  in  some  cases  both  are  typical  teeth  (Fig.  220). 
The  second  germ  may  develop  an  atypical  tooth  or  one  but  slightly 


MACROSCOPIC  MALFORMATIONS 


267 


abnormal  in  form.    The  geminous  teeth  may  nndergo  fusion,  as  seen 

in  Fig.  216,  A, 

DupUcation  of  the  Pulp  Cavity.— Hopewell-Smith  calls  attention 
to  a  case  of  an  upper  permanent  central  incisor  containing  two  pulp 
cavities  in  the  coronal  portion,  probably  an  interrupted  gemination. 

Fig.  220 


Double  gemmation  of  upper  permanent  lateral  incisiors. 

Dilaceration.— By  dilaceration  is  meant  a  displacement  of  a  formed 
portion  of  a  tooth  in  such  a  manner  as  to  change  its  relative  position 
to  the  soft  parts  engaged  in  its  development,  the  development  then 
being  continued  in  the  new  relation.^  For  example,  an  accident  to 
a  temporary  tooth  occurs  and  the  force  may  displace  the  partially 
formed  permanent  crown,  altering  its  relation  to  the  enamel  organ 
and  papilla  engaged  in  its  formation.  The  balance  of  the  crown 
may  be  formed  in  the  new  situation  and  be  of  fairly  perfect  or  of 
imperfect  structure  (Fig.  221).  This  is  most  likely  to  occur  with 
the  anterior  teeth,  especially  when  a  temporary  tooth  is  driven  mto 
the  alveolar  process,  its  root  in  turn  displacing  the  permanent  tooth, 
thus  twisting  its  relation  to  its  formative  organs. 

Flexion. — Flexion  means  the  movement  of  one  of  the  formative 
organs  of  a  tooth  away  from  its  normal  relation  to  the  hard  part  it 
is  developing.  The  soft  part  has  its  position  altered,  the  hard  part 
remaining  in  correct  position.  Subsequent  formations  therefore 
have  an  abnormal  relation  to  the  previously  formed  portions  of  the 
tooth. 

As  an  example  of  flexion,  a  portion  of  the  enamel  organ  of  a  tooth 
may  be  displaced  and  in  its  new  relations  may  form  enamel  in  an 

1  Tomes. 


268     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 


unusual  situation,  as,  for  example,  upon  the  side  or  neck  of  the  root 
(see  enamel  nodule)  or  even  in  the  bifurcation  or  on  the  apex  of  the 
root  (Figs.  222  and  225).  Again,  it  is  probable  that  lack  of  space 
may  cause  deflection  of  a  pulp  engaged  in  root  formation,  a  curved 
root  being  the  result  (Fig.  231).  The  pericementum  (follicle  wall) 
moves  with  the  pulp  in  these  cases. 


Fig.  221 


Pulp  hernia  and  flexion,  mesiodistal 
section:  E,  enamel,  distal  section  in  the 
bifurcation  of  the  roots;  D,  dentin;  C, 
C,  cementum;  PC,  pulp  cavity;  F,  large 
apical  foramen :  B  of  R,  bifurcation  of  the 
roots.    (From  a  specimen,  enlarged.) 


Fig.  223 


^^^S^!^-- 


Dilaceration.  Shows  fold  in  the  labial 
enamel  and  cervical  dentin.  (After  von 
Wunschheim.i) 


Enamel  excrescences.     (Salter.) 


Unusual  Locations  of  Enamel. — That  during  development,  the  enamel 
organ  or  portions  of  it,  may  assume  an  abnormal  relation  to  the  pulp, 
is  evidenced  by  odontomes.  Apart  from  these,  there  are  evidences 
seen  in  teeth  which  show  that  portions  of  the  enamel  organ  may 
become  detached  from  the  main  organ,  and  develop  enamel  in  unusual 
situations.  Thus  columns  of  enamel  may  penetrate  the  body  of  the 
dentin. 

A  small  nodule  or  cap  of  enamel  overlying  dentin,  and  itself  over- 
lapped at  the  edges  by  cementum  (Fig.  226),  may  be  found  upon  the 
root  of  a  molar,  usually  upon  the  side  of  an  upper  third  molar  at  a 


1  G.  von  Wunschheim:  Fracturen,  Infraktionen  und  Knickungen  der  Zahne. 


MACROSCOPIC  MALFORMATIONS 


269 


point  about  one-eighth  inch  from  the  cervical  margin  of  the  crown 
enamel;  but  one  may  be  one-half  inch  distant  from  the  enamel  mar- 


FiG.  224 


Fig.  225 


Lower  molar  with  enamel  nodule 
connected  to  the  enamel  of  crown  by 
a  ridge  enamel. 


Five-rooted  upper  molar,  cap  of  enamel 
on  end  of  one  root. 


gin.  A  thin  ridge  of  enamel  sometimes,  though  not  usually,  seen 
connecting  them,  indicates  the  nodule  to  have  been  formed  by  a 
detached  portion  of  the  original  enamel  organ  (Fig.  224).    This  forma- 


FiG.  226 


Structure  of  enamel  nodule.     E,  enamel;  D,  D,  dentin.     (Hopewell-Smith.) 

tion  is  known  as  an  enamel  nodule.     It  may  occur  upon  a  lower 
molar,  though  usually  found  upon  the  upper  molars.     Twomay 


270     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

exist  on  opposite  sides  of  a  molar,  as  in  a  specimen  possessed  by  the 
editor.    They  may  cause  neuralgia.     (Ottofy.) 

A  molar  root  may  have  a  cap  of  enamel  upon  its  apex,  an  evidence 
of  extreme  displacement,  even  more  than  shown  in  Fig.  225.  Some- 
times an  enamel  ridge  runs  down  the  side  of  a  root;  sometimes  an 
excrescence  may  be  found  upon  the  enamel  (Fig.  223).     Fig.  222 


Fig.  227 


Fig.  228 


Fig.  229 


Upper  molar 
with  supplemental 
cusp  on  lingual 
side. 


Showing  talon-like  un- 
usual development  of 
the  cingule  on  an  incisor. 
(From  case  reported  by 
W.  H.  Mitchell,  Dental 
Cosmos,  vol.  xxxiv.) 


Very  large  supplemental  cusp 
on  the  buccal  surface  of  upper 
molar.  Probably  a  fused  "para- 
molar." 


shows  enamel  formed  in  the  bifurcation  of  the  roots  of  a  lower 
molar.  This  enamel  nodule  has  been  explained  upon  the  hypothesis 
that  the  remains  of  the  epithelial  root  sheath  of  Hertwig  have  within 
them  the  inherent  power  of  forming  enamel,  which  may  account 
for  enamel  on  the  side  or  end  of  a  root.    As  this  epithelial  root-sheath 


Fig.  2.30 


Fig.  231 


Fig.   232 


Cuspids  with  long  roots. 


Curved  roots.  Upper  cuspid  with  two  roots. 


is  probably  the  trailing  remains  of  the  enamel  organ  left  as  the 
organ  is  carried  up  by  the  tooth,  it  is  quite  likely  that  larger  portions 
of  the  organ  may  be  detached  as  above  explained.     (See  Fig.  98.) 

Supplemental  Cusps. — Occasionally  a  tooth  has  a  greater  number  of 
cusps  than  usual.  The  most  common  form  of  this  condition  is  a 
supplemental  mass  attached  to  the  palatal  side  of  the  mesopalatine 


MACROSCOPIC  MALFORMATIONS 


271 


cone  of  the  upper  first  molars  (Fig.  227).  It  is  more  rarely  the  case 
that  a  cingule  of  this  sort  is  noted  upon  the  lower  molars.  The 
palatal  tubercle,  the  prominence  upon  the  cingule  of  an  upper  incisor, 
may  be  of  exaggerated  size.     In  one  case  (Fig.  228)  this  develop- 


FiG.  2.33 


Fig.  234 


Fig.  235 


Short  buccal  root  of  a 
molar,  otherwise  properly 
developed. 


Central  incisor  with 
short  root. 


Five-rooted  upper  third 
molar. 


Fig.  236 


ment  gave  the  appearance  of  a  talon  upon  the  tooth,  a  distinct  cusp 
segment  in  itself.  Fig.  229  illustrates  a  marked  supplemental  cusp 
upon  the  buccal  surface  of  a  molar.  A  fusion  in  this  location  is  not 
impossible.     (See  Fourth  Molar.) 

Malformations  of  Roots. — Differences  in  regard 
to  the  size,  arrangement,  form,  and  number  of 
the  roots  of  teeth  are  the  most  common  of  the 
dental  malformations.  The  roots  of  teeth  may  be 
abnormally  long  (Fig.  ^230)  or  abnormally  short 
(Figs.  2.33^ and  234). 

The  roots  of  cuspids  may  be  bifurcated,  par- 
ticularly in  the  lower  jaw  (Fig.  232).  A  central 
may  have  a  short  supplemental  root.  (Guil- 
ford^), or  sometimes  two  distinct  roots  as  in 
Fig.  236. 

The  upper  first  bicuspids  may  have  trifurcated 
roots,  the  extra  root  usually  being  on  the  buccal 
aspect.    The  upper  second  bicuspid  may  be  bifur- 
cated; upper  molars  may  have  more  than  three 
roots,  the  third  molar  often  having  four,  five,  or 
six,  and  in  one  case  reported,  eight  roots  (Figs.  225  and  235).    In 
some  cases  upper  third  molars  have  but  one  root  Avith  a  single,  large 
canal,  a  case  of  true  developmental  fusion.    In  other  cases  the  roots 
are  fused  so  as  to  form  apparently  but  one  root,  while  the  canal 


Two-rooted  upper 
right  central  incisor. 
(Warren. 2} 


1  American  System  of  Dentistry. 

2  Dental  Brief,  April,  1913. 


272     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

divisions  may  exist.  This  may  be  fusion  or  concrescence  of  roots. 
Lower  molars  may  have  three  or  four  distinct  roots,  but  rarely  only 
one. 


Fig.  237 


Fig.  238 


Fig.  239 


Fibrous  odontome. 
(Garretson,  after 
Pierce.) 


Two-rooted  lower  cuspid. 
Resorption  of  temporary 
roots.  (Skiagraph  by  E. 
Ballard  Lodge.) 


Results    of    hernia   of   a 
pulp.     (Salter.) 


Fig.  240 


Fig.  239  magnified. 


MACROSCOPIC  MALFORMATIONS 


273 


Abnormalities  of  root  form  are  of  extreme  frequency,  and  are 
probably  explained  upon  the  hypothesis  of  flexion  of  the  root  pulp, 
previous  to  the  deposition  of  the  curved  portion  of  root  tissue. 

It  is  impossible  to  diagnose  the  forms  of  roots  from  the  appear- 
ance of  the  crowns,  but  a  skiagraph  will  determine  their  form  with 
certainty.  It  may  be  said,  however,  that  narrow  necks  indicate  a 
probable  divergence  of  roots,  and  vice  versa. 

An  excrescence  upon  the  cementum  is  known  as  a  cemental  nodule. 

Odontomata.^ — An  odontoma  is  a  growth  composed  of  structures  of 
which  the  teeth  are  composed,  but  the  masses  may  be  so  arranged 
as  to  have  no  typical  form  or  even  resemblance  to  a  tooth.  They  may 
appear  in  the  arch  or  may  remain  embedded  in  the  jaw,  where  they 
may  lie  quiescent  or  may  excite  cyst  formation  (Fig.  31),  or  give  rise 
to  various  morbid  reactions,  such  as  tumor  formation. 

It  has  been  held  by  Broca  that  any  of  the  formative  organs  of  the 
tooth- — enamel  organ,  dentinal  papilla,  or  follicle  wall — may  undergo 
aberrant  development  and  may  thereafter  deposit  calcific  tissue  or 
not,  as  the  case  may  be.  If  not,  soft  tumors  of  the  jaw,  not  dis- 
tinctly dental,  may  form,  though  in  its  complete  form  such  a  tumor 
may  become  a  seat  of  calcific  deposition  peculiar  to  the  aberrant 
tissue. 

Fig.  241  Fig.  242 


Radicular  odontome.     (Tomes.) 


Odontoma.     (Garretson.) 


Bland  Sutton's  classification  is  usually  adopted,  and  is  as  follows: 

1.  Aberrations  of  the  enamel  organ:     (a)  Epithelial  odontomes. 
(6)  Calcified  epithelial  odontomes. 

2.  Aberrations  of  the  follicle:     (a)  Follicular  cysts.     (6)  Fibrous 
odontomes.    (c)  Cementomata.    (d)  Compound  follicular  odontomes. 

3.  Aberrations  of  the  papilla :  (a)  Radicular  odontomes.    (6)  Den- 
tomata.     (c)  Osteodentomata.     (d)  Cementomata. 

4.  Aberrations    of    the    whole    tooth  germ   (or  three  formative 
organs),  composite  odontomes. 

The    Uncalcified  Odontomata:     1.  Epithelial   odontomata  which 
arise  by  aberrant  development  of  the  enamel  organ,  and  remaining 
uncalcified  resemble  the  adenomata. 
18 


274     MALFORMATIONS  AND  MALPOSITIONS  OF  THE   TEETH 

2.  Follicular  odontomata:  (a)  The  wall  of  the  follicle  is  distended 
and  the  cavity  is  filled  with  a  thick  fluid  (sometimes  pus  if  infected), 
and  contains  a  portion  of  imperfectly  developed  tooth.  It  is  in  this 
form  really  a  cyst  (Fig.  31).  (b)  The  follicle  wall  or  pericementum 
may  thicken  so  as  to  form  a  fibrous  capsule  about  the  tooth,  suffi- 
ciently resistant  to  prevent  its  eruption  (Fig.  237).  This  is  called 
a  fibrous  odontome. 

3.  Compound  follicular  odontomata:  The  follicle  wall  thickens 
into  a  fibrous  capsule,  and  in  this  may  appear  fragments  of  cemen- 
tum,  dentin,  or  imperfectly  formed  teeth  with  their  enamel,  dentin, 
and  cementum. 

Fig.  243 


Composite  odontome.     (Garretson.) 


It  is  a  combination  of  an  uncalcified  and  calcified  form,  and  might 
easily  lead  to  formation  of  a  cyst  containing  many  teeth  or  portions 
of  teeth. 

The  Calcified  Odontomata:  1.  Epithelial.  The  enamel  organ 
develops  aberrantly  into  a  large,  possibh^  multilocular  mass,  and 
enamel  deposition  occurs. 

2.  The  Cementomata:  A  fibrous  odontome  forms  from  the  follicle 
wall,  then  calcifies  into  laminated  ossific  material.  One  from  a 
horse,  in  the  Royal  Veterinary  College,  London,  weighed  seventy 
ounces.    It  may  include  one  or  more  teeth. 

3.  Radicular  Odontomata:  The  crown  may  form  normally,  but 
the  dentinal  papilla  becomes  aberrant  and  develops  largely,  conveying 
with  it  the  follicle  wall.     Ceasing  to  enlarge,  cementum  and  dentin 


MACROSCOPIC  MALFORMATIONS 


275 


are  deposited  somewhat  in  the  ordinary  manner,  bnt  of  somewhat 
aberrant  deposition.  Pulp  hernia  comes  under  this  heading  and 
acts  similarly  (Figs.  239,  240,  and  241). 

4.  Composite  Odontomata:  The  developmental  organs,  the 
enamel  organ,  the  papilla,  and  follicle  wall  are  aberrant,  hetero- 
geneously  arranged,  enlarged,  and  then  deposit  a  composite  mass, 
which  may  be  somewhat  orderly  and  tooth-like  (Fig.  242),  or  be 
totally  unlike  a  tooth  as  in  Fig.  244. 

The  diagnosis  of  odontoma,  if  at  all  obscure  may  be  made  by 
skiagraphy  (see  Fig.  245). 

Fig.  244 


Composite  odontome.     (Garretson.) 


Treatment. — The  treatment  of  odontomata  is  usually  that  directed 
to  their  sequels,  which  consist  of  enlargements  about  the  jaws  with 
more  or  less  inflammation  or  cyst  formation,  and,  as  a  rule,  involves 
their  removal  by  surgical  operation. 

Anomalies  of  Number. — Although  the  dental  series  of  man  nor- 
mally consists  of  thirty-two  members,  cases  are  frequently  observed 
in  which  the  number  is  less  than,  or  in  excess  of  that  number,  or  there 
is  an  abnormal  number  in  any  particular  group  of  teeth. 

Deficiency. — It  is  observed  with  some  frequency,  that  the  upper 
lateral  incisors  never  make  their  appearance,  a  condition  traceable  to 
the  influence  of  heredity  in  some  of  the  instances.  In  an  interesting 
case  of  three  sisters,  who  all  were  without  upper  laterals,  a  son  of  one 
of  them  had  them.  Unfortunately  the  history,  as  to  the  parents  of 
the  sisters,  was  not  certain,  as  they  wore  artificial  teeth. 

When  the  laterals  are  absent,  the  permanent  cuspid  erupts  and 
occupies  the  lateral  incisor  space,  and  thus  sometimes  fails  to  cause 
resorption  of  the  root  of  the  temporary  cuspid,  which  persists  in  the 


276      MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

cuspid  space  (Fig.  153).  The  lower  laterals  sometimes,  but  more 
rarely,  fail  to  appear;  are  probably  never  formed  (Fig.  247).  The 
third  molar  may  never  appear,  or  appear  as  a  peg-like  tooth. 

The  cuspid  often  is  impacted  but  is  seldom  lacking  in  formation. 
Usually  when  missing  it  is  to  be  found  by  skiagraphy. 

Fig.  245 


Surgical  fracture  of  mandible,  with 
photograph  of  odontoma  and  molar 
tooth  after  removal.     (Graham.) 


The  cases  of  suppressed  teeth, 
next  in  point  of  frequency,  are 
those  of  the  bicuspid  teeth.  If 
the  corresponding  teeth  are  all 
present  in  the  dental  arch,  a 
well-founded  suspicion  of  impac- 
tion of  the  missing  tooth  may  be 
entertained. 

An  excessive  growth  of  hair  upon  the  face  and  body  has  also  been 
associated,  in  some  cases,  with  a  deficiency  in  number  and  altera- 
tion in  form  of  the  teeth.  In  other  cases  no  abnormality  was  notice- 
able.^ In  some  cases  the  hair  and  other  dermal  structures  may  be 
normal  and  the  teeth  be  quite  deficient  in  number. 

The  extreme  of  suppressed  formation  is  represented  in  a  case 
described  by  Guilford. ^ 


1  Tomes :  Dental  Surgery. 


2  American  System  of  Dentistry,  vol,  iii. 


MACROSCOPIC  MALFORMATIONS 


277 


A  patient  over  fifty  years  old  had  never  erupted  any  teeth,  tem- 
porary or  permanent;  the  alveolar  arches  revealed  no  evidences  of 


Fig.  246 


Structure  of  a  composite  odontome.     (Garretson.) 
Fig.  247 


Absence  of  both  upper  and  lower  laterals  in  the  same  mouth.     Temporary  left  upper 

cuspid. 

enclosed  teeth,  but  had  the  appearance  of  typical  edentulous  jaws; 
the  alveolar  bone  itself  was  but  primitive.    The  case  appeared  to  be 


278      MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

sporadically  hereditary,  a  grandparent  and  an  uncle  exhibiting  a 
like  condition.  The  cases  are  interesting  also  because  of  additional 
evidences  of  faulty  evolution  of  dermoid  structures.  In  the  first 
case  cited,  no  sudoriparous  glands  appear  to  have  formed,  and  there 
was  but  a  faint  growth  of  hair  on  the  cranium,  and  none  on  the 
face  and  body.  The  uncle  was  hairless  and  edentulous  from  birth. 
Guilford  found,  in  other. members  of  the  family,  an  absence  of  the 
full  complement  of  teeth. 

In  an  interesting  summary,  Kjaer^  quotes  Trueswell  as  knowing 
of  a  man,  aged  fifty-four  years,  having  had  no  permanent  teeth,  but 
all  of  his  temporary  ones,  and  Fricke  as  having  3  cases  of  retention 
of  temporary  teeth  until  sixteen,  eighteen,  and  twenty  years  respec- 

FiG.  248 


Malposition  of  molar  teeth. 

tively,  when  the  permanent  teeth  appeared,  and  Linderer  as  having 
a  case  of  a  lady,  aged  sixty  years,  who  never  had  any  teeth,  and  a 
case  of  his  own  in  which  the  temporary  teeth  were  lost  from  time  to 
time,  but  no  permanent  successors  appeared,  and  none  could  be 
detected  by  skiagraphy.  He  attributed  the  lack  to  some  disturbance 
during  fetal  life,  as  the  family  history  did  not  include  such  a  case. 

Excess. — The  possible  occurrence  of  a  condition  in  some  respects 
the  reverse  of  the  preceding,  has  been  much  written  of  and  discussed 
— i.  e.,  the  occurrence  of  a  complete  third  denture.  There  can  be  but 
one  conclusion  from  an  examination  of  all  the  evidence  thus  far 
presented,  and  that  is  that  no  clear  and  well-authenticated  cases  are 

1  Dental  Cosmos,  1907. 


MACROSCOPIC  MALFORMATIONS  279 

made  out.  Isolated  cases  of  the  appearance  of  teeth  su})seqiient  to 
the  loss  of  all  of  the  second  denture  are  not  infrequent;  and,  so  far 
as  clear  records  can  be  obtained,  are  resolvable  into  cases  of  the 
eruption  of  supernumerary  or  impacted  teeth,  though  sometimes 
a  number  of  teeth  are  reported  erupted.  While  these  cases  are, 
at  least  for  the  present,  to  be  held  as  unproved  in  connection  with 
elderly  persons,  a  well-authenticated  case  of  multiple  dentition  in 
a  child  is  recorded  by  Catching.^  Between  the  sixth  and  seventh 
month  the  eruption  of  one  set  of  teeth  was  complete;  within  three 
months  all  of  these  had  been  lost.  Between  the  eleventh  and  fifteenth 
months  another  period  of  dentition  occurred,  the  teeth  of  this  second 
denture  being  of  such  faulty  structure  as  to  crumble  away  quickly. 
At  the  age  of  two  and  one-half  years  a  third  dentition  appeared, 
which  caused  the  child  such  inconvenience  that  the  teeth  were 
extracted  by  the  mother.  At  the  age  of  eleven  years  a  fourth  series 
erupted,  incomplete  through  the  absence  of  six  teeth.  At  the  age  of 
fifteen  years  these  teeth  were  sound  and  firm. 

The  Fourth  Molar. — Very  rarely  a  fully  developed  fourth  molar 
appears  in  the  maxilla.  In  one  case  it  was  impossible  to  distinguish 
the  normal.  The  third  and  fourth  lay  in  lingual  and  buccal  relation. 
Less  rarely,  a  less  typical  molar  appears  posterior  to  the  third  molar. 
This  must  be  very  rare  in  lower  molars.  A  third  type  of  super- 
numerary appears  in  the  maxilla.  These  are  rudimentary,  and 
appear  upon  the  buccal  side,  opposite  the  approximation  of  the 
first  and  second  molars  or  of  the  second  and  third  molars,  or  to  the 
distal  or  distolingual  of  the  third  molars.  Bolk^  calls  the  buccal 
supernumerary  the  "paramolars,"  and  says  they  are  small,  two- 
cusped,  single  rooted,  and,  if  fused,  usually  unite  with  the  mesio- 
buccal  portion  of  the  tooth  posterior  to  it  during  development.  Here 
it  forms  a  supplemental  section,  "paramolar  tubercle"  (Fig.  229), 
which  may  have  a  distinct  ''paramolar  root"  or  root  indication.  Bolk 
accounts  for  the  less  frequent  appearance  of  an  anterior  independent 
paramolar  (opposite  the  approximation  of  the  first  and  second  molars) 
upon  the  supposition  of  a  more  frequent  fusion  with  the  second  molar, 
and  he  has  found  twice  as  many  ''paramolar  tubercles"  in  the  second 
molar  as  in  the  third.  The  supernumerary  posterior  of.  the  third 
molar  he  terms  the  "  distomolar,"  and  finds  that  when  fused,  it 
unites  with  the  distolingual  section  of  the  third  molar.  He  has  noted 
a  rare  case  having  both  a  paramolar  and  distomolar.  He  also  has 
not  observed  independent  paramolars  in  the  mandible,  bnt  the  para- 

1  Southern  Dental  Journal,  October,  1886. 

2  For  the  many  beautiful  illustrations  enforcing  this  new  conception  the  reader  is 
referred  to  the  article  in  Dental  Cosmos,  February,  1914. 


280     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

molar  tubercle  may  occur  on  the  second  or  third  molars,  which  may 
have  a  proper  "paramolar  root."  The  distomolar  in  the  mandible 
fuses  with  the  distolingual  portion  of  the  third  lower  molar.  He 
calls  attention  to  the  fact  that  in  the  maxilla,  the  paramolar  appears 
most  often  as  a  supernumerary  tubercle,  while  in  the  mandible  it  is 
emphasized  by  a  supernumerary  root. 

Supernumerary  Teeth. — Any  teeth  in  excess  of  the  normal  number 
of  teeth  belonging  to  any  one  class  are  included  in  the  category  of 
supernumerary  teeth.  The  number  of  teeth  may  possibly  not  exceed 
thirty -two.  Supernumerary  teeth  appear  as  simple  unmodified 
cones,  or  as  combinations  of  cones  resembling  the  forms  of  teeth. 
The  conical  form  is  most  common.  Cases  where  these  peg-like  teeth 
appear  around  the  third  molars,  singly  or  in  number,  are  numerous. 
Their  appearance  in  any  situation  is  evidence  that  the  normal  number 
of  dental  cords  has  been  exceeded. 

Fig.  249 


The  fourth  molar     (Hartman.) 


Guilford^  divides  supernumerary  teeth  into  those  having  typical 
anatomical  forms  and  those  having  atypical  forms. 

Supernumerary  incisors  having  typical  forms  appear  in  either 
jaw.  In  the  upper  jaw,  supernumerary  centrals  and  laterals  both 
appear,  the  latter  more  frequently  (Fig.  220).  Supernumerary  teeth 
may  occupy  any  position  relative  to  the  dental  arch,  but  are  more 
frequently  seen  at  its  lingual  side.    The  compound  cone  occasionally 

1  American  System  of  Dentistry,  vol.  iii. 


MACROSCOPIC  MALFORMATIONS 


281 


appears  (Fig.  251).     In  addition  to  molars  and  incisors,  supernu- 
merary bicuspids  are  occasionally  found  (Fig.  232) ;  supernumerary 


Fig.  250 


Two   atypical   upper  supernumerary  teeth  displacing  the  incisors. 


Fig.  251 


cuspids  are  very  rare,  but  sometimes  a  brood  of  them  exists,  as  many 
as  seventeen  fairly  defined  small  teeth  having  been  removed  from  a 
cyst  in  the  location  of  the  cuspid  tooth. ^ 

Unless  supernumerary  teeth  are  a  source  of  offence, 
either  through  their  position  or  appearance,  they 
need  not  be  disturbed.  If  they  are  found  to  be  so, 
they  should  be  extracted. 

Malpositions  of  the  Teeth. — A  tooth  is  said  to  be 
in  malposition  when  it  is  not  in  normal  relation  with 
the  dental  arch  to  which  it  belongs  and  to  its 
antagonizing  teeth  of  the  opposing  arch.  Teeth  are 
found  in  abnormal  positions  as  the  result  of  a  variety 
of  causes.  Some  of  these  operate  prior  to,  during,  or 
immediately  after  eruption;  some  long  after  the  eruption  of  the 
teeth,  and  some  because  of  non-eruption  of  teeth.    (See  p.  220,  etc.) 

Malpositions  which  are  remediable  through  the  application  of 
mechanical  force,  applied  by  means  of  suitable  apparatus,  belong  to 
operative  dentistry,  as  has  been  stated.  They  are  fully  treated  of  in 
works  upon  operative  dentistry^  and  orthodontia.^ 

>  D.  M.  Clapp:  International  Dental  Journal,   1900. 

^  American  Test-book  of  Operative  Dentistry.  ^  Guilford,  Angle,  and  others. 


The  compound 
cone. 


282     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

The  extraction  of  teeth  after  they  have  })een  erupted,  or  of  their 
predecessors,  is  one  of  the  most  frequent  causes  of  acquired  mal- 


FiG.  252 


Fig.  253 


Case  of  seven  lower  bicuspids,  two  supernumeraries  in  place  and  one  erupting.  This 
patient  has  two  supernumerary  upper  central  incisors  displacing  the  centrals  proper, 
yet  closely  resembling  them. 

position  of  the  remaining  teeth.  The  teeth  move  from  their  original 
positions,  the  anterior  teeth,  incisors,  laterals,  cuspids,  and  occa- 
sionally the  bicuspids,  having  a  tendency  to  drift  posteriorly,  some- 
times opening  a  space  between  the  central  in- 
cisors, sufficiently  large  to  create  a  deformity. 
The  molars  have  a  decided  natural  tendency 
to  drift  forward,  and  when  the  bicuspids  are 
removed  they  tip  anteriorly,  causing  maloc- 
clusion upon  their  distal  cusps  and  sometimes 
their  distobuccal  cusps  alone,  with  a  further 
tendency  to  tip  forward  and  sometimes  inward 
as  well.  Separation  of  the  posterior  teeth  may 
occur,  and  in  any  event,  the  loss  of  mesial  or 
distal  support  permits  fibrous  food  to  be  packed 
between  the  teeth;  as  they  spring  slightly  apart, 
it  is  held  by  their  springing  together  again. 
The  lack  of  occlusion  brought  about  by  extrac- 
tion of  antagonists  permits  elongation,  and  the 
loss  of  posterior  support  is  apt  to  bring  about  labial  protrusion  or 
abrasion  of  upper  anterior  teeth.     This  effect  is  produced  in  youth 


Effects  of  premature 
loss  of  permanent  first 
molars. 


IMPACTION  OF  TEETH  283 

when  the  first  molars  are  lost  before  the  bicuspids  are  in  place  (Fig. 
253).  The  first  molars  are  the  keystones  of  the  arches,  and  determine 
the  extent  of  the  formative  process  which  shall  occur  in  the  alveolar 
bone  posterior  to  them.  They  are  also  the  teeth  which,  correctly 
placed  or  out  of  position,  determine  largely  the  occlusion  of  the  teeth. ^ 

If  a  temporary  tooth  be  long  retained,  it  is  sometimes  raised  to 
the  occlusal  level  of  the  other  teeth;  again,  it  is  sometimes  left  at  its 
original  level  and  occasionally  imprisoned  between  other  teeth.  The 
a;-rays  should  be  used  to  determine  the  presence  or  absence  of  the 
permanent  tooth  germ  or  resorption  of  the  temporary  roots. 

If  teeth  erupt  in  malposition,  it  is  held  to  be  wuse  to  correct  as 
early  as  possible,  in  order  to  prevent  further  malposition  of  other 
teeth. 

Fig.  248  illustrates  a  case  of  malposition  of  molar  germs  which  have 
developed  in  the  incisal  region,  displacing  the  incisors. 

Impacted  and  Encysted  Teeth. — The  extreme  extent  of  dental 
malposition  is  reached  when  the  permanent  teeth  do  not  erupt  at 
all.  Instead  of  presenting  in  the  dental  arch,  they  may  be  entirely 
embedded  in  the  substance  of  the  bone,  either  remaining  there,  with 
or  without  pathological  manifestations,  or  erupting  in  some  unusual 
situation.  In  other  cases,  a  distinct  cystic  tumor  forms  about  the 
enclosed  tooth  (Fig.  31).  The  cause  of  impaction  probably  lies 
either  in  a  previous  malposition  of  other  teeth  preventing  advance, 
or  in  an  originally  malposed  tooth  germ,  or  to  the  development 
of  the  root  while  the  crown  advance  is  retarded,  the  expulsive 
force  of  root  formation  being  lost.  In  many  cases  orthodontic 
procedures  creating  room  may  permit  the  descent  of  the  tooth. 

Impacted  Lower  Third  Molars. — By  far  the  most  common  dental 
impaction  is  that  of  the  lower  third  molar.  The  extent  of  impaction 
varies  from  a  partial  eruption,  or  partial  imprisonment  of  the  tooth  by 
its  bony  surroundings,  to  its  entire  imprisonment  in  any  part  of  the 
ramus.  Many  of  the  more  severe  cases  treated  under  the  head  of 
pathological  dentition,  if  unrelieved,  would  be  included  in  the  category 
of  impacted  teeth. 

In  Fig.  254  is  shown  a  lower  third  molar  presenting  the  effects  of 
a  previous  impaction.  The  irritation  caused  by  the  efi^orts  of  the 
tooth  to  disengage  itself,  or  to  overcome  the  resistance  to  its  erup- 
tion, has  caused  an  active  formative  reaction  in  the  pericementum, 
resulting  in  an  hypertrophy  of  the  cementum.  Likewise  the  pressure 
upon  the  bone  causes  a  condensing  osteitis,  and  the  bone  becomes 
dense,  more  obstructive,  and  less  vascular  (see  p.  144). 

1  Angle. 


284     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

If  the  distance  between  the  posterior  surface  of  the  second  molar 
and  the  columns  of  the  coronoid  process  be  very  short,  it  is  evident 

Fig.  254 


Right  hal  iof  lower  jaw,  showing  an  impacted  third  molar.    (Cryer.) 
Fig.  255 


Inner  side  of  left  half  of  same  lower  jaw.      (Cryer.) 


that  upward  eruption  is  impossible,  so  that  the  tooth  may  assume 
any  direction  of  movement,  the  most  common  being  forward,  the 


IMPACTION  OF  TEETH 


285 


axis  of  the  tooth  changing  its  position  until  the  tooth  may  He  in  a 
horizontal  position  or  even  become  inverted. 


Fig.  256 


Impaction  of  lower  third  molar.     Resportion  of  root  of  second  molar  and  impingement 
of  root  upon  inferior  dental  canal,  which  is  deflected  out  of  its  course.     (Cryer.) 

Fig.  255  is  taken  from  the  same  jaw  as  Fig.' 254,  but  shows  the 
opposite  side;  the  impaction  is  pronounced.  Fig.  256  shows  another 
case  with  different  anatomical  surroundings.  In  the  first  case  there 
were  evidences,  both  in  the  tooth,  in  its  bony  surroundings,  and  in 
the  external  cortical  bone,  of  the  results  of  the  irritation  produced 
by  the  efforts  at  eruption.  The  cementum  was  thickened;  the  outer 
follicular  wall,  the  tissue  designed  to  form  the  alveolar  periosteum, 


Fig.  2.57 


Fig.  258 


Impacted  lower  third  molar  beneath  gum. 
Second  molar  tipped  forward.  (Skiagraph 
by  E.  Ballard  Lodge.) 


Impacted  cuspid.     (Skiagraph  by  E. 
Ballard  Lodge.) 


had  exercised  its  formative  osteogenetic  function,  and  a  capsule  of 
bone  had  formed  about  the  tooth;  it  lay  in  a  bony  chamber.    The 


286     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

pressure  exerted  upon  the  distal  wall  of  the  second  molar  had  resulted 
in  a  pressure  resorption  of  its  root  until  the  pulp  chamber  was 

Fig.  259 


Impacted  bicuspid.    (Skiagraph  by  E.  Ballard  Lodge.) 

encroached  upon.    These  were  both  postmortem  cases,  and  no  records 
of  their  clinical  histories  were  obtainable.    The  symptoms  produced^ 

Fig.  260 


Same  as  shown  in  Fig.  234,  with  tooth  removed.     (Cryer.) 


could  only  be  surmised  b}^  the  nature  of  the  anatomical  relations 
and  the  pathological  evidences.    There  may  have  been  a  prolonged 


IMPACTION  OF  TEETH 


287 


but  mild  periostitis,  probably  a  continued  pulp  irritation;  and  in  the 
last,  neuralgia  of  any  grade  of  severity.    The  pressure  upon  nerves 


Fig.  261 


Wisdom  teeth  embedded  in  the  rami  of  the  lower  jaw.     (Tomes.) 

of  the  inferior  dental  canal  would  account  for  neuralgia  or  mental 
or  other  disturbance. 

Cryer    calls    attention    to   the  ^'°-  ^^^ 

fact  that  a  third  lower  molar  in 
its  attempt  to  erupt,  frequently 
causes  a  cellulitis,  extending  into 
the  temporomandibular  joint, 
causing  acute  ankylosis.^ 

Judging  from  postmortem  re- 
cords and  recent  skiagraphy, 
cases  of  impacted  third  molars 
are  more  common  than  generally 
believed.  Instead  of  remaining 
in  the  alveolar  portion  of  the 
bone,  the  impacted  tooth  may 
come  to  occupy  a  cavity  in  some 
portion  of  the  body  or  the  ramus 
of  the  bone  (Figs.  261  to  264). 
The  positions  of  the  teeth  in 
such  cases  tend  to  confirm 
Tomes'  theory  of  the  develop- 
ment of  the  jaw.  The  jaw  being  lengthened,  and  the  ramus  develop- 
ing through  conjoined  deposition  and  resorption  of  bone,  the  crown 
of  the  tooth  appears  to  be  either  fixed  in  a  bony  nucleus  and  trans- 
ported to  some  distant  point  in  the  developmental  progress  of  the 
jaw,  or  to  be  irregularly  shifted  about  during  jaw  growth.    At  later 


Wisdom  tooth  buried  in  the  ramus. 
(Tomes,  after  Marshall.) 


'  Dental  Cosmos,  October,  1911. 


MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

periods,  the  pressure  exercised  by  root  formation  disturbs  the  rela- 
tions of  the  tooth  with  its  earher  surroundings.  These  efforts  at 
eruption  may,  at  late  periods,  cause  the  appearance  of  the  tooth  in 
odd  situations.  In  the  case  shown  in  Fig.  263  the  crown  of  the 
tooth  made  its  way  through  the  angle  of  the  bone  and  through  the 
muscles  and  skin.  The  opening  in  the  skin  healed  upon  extraction 
of  the  tooth. 

Impacted  Upper  Third  Molars. — ^Some  phases  of  impaction  of  this 
tooth  have  been  spoken  of  under  the  head  of  Pathological  Dentition. 
The  most  common  is  imprisonment  of  the  tooth  and  its  subsequent 
partial  eruption  in  a  horizontal  position,  the  crown  pointing  toward 
the  cheek  (Fig.  173).  The  crown  of  this  tooth  may,  in  rare  cases,  be 
directed  inward  or  backward,  in  the  latter  case  being  arrested  by 
the  pterygoid  plates  of  the  sphenoid  bone.  It  may  present  with 
an  anterobuccal  facing  of  the  crown,  as  shown  in  Fig.  264,  or  with 
a  posterobuccal  facing. 

Fig.  263 


From  a  wax  model  in  the  museum  of  the  London  Odontological  Society.    (Tomes.) 

In  a  case  recorded  by  Tomes  (Fig.  265)  the  extraction  of  the 
second  molar  revealed  the  third  molar  in  a  reversed  position,  its 
roots  occupying  the  depression  between  the  roots  of  the  second 
molar.  A  case  has  been  reported,  of  an  upper  molar  with  the  roots 
partly  embedded  in  the  floor  of  the  antrum,  its  neck  carious,^  and 
the  antrum  in  a  state  of  suppuration. 

Impacted  Cuspids. — In  point  of  frequency  of  impaction  the  upper 
cuspids  stand  next  to  the  lower  third  molars.  The  upper  cuspids  lie 
high  up ;  the  floors  of  their  crypts,  in  which  they  lie  loosely,  are  at  a 
higher  level  than  those  of  the  adjoining  teeth;  their  crowns,  as  with 
the  other  anterior  teeth,  lie  lingual  to  the  roots  of  their  predecessors. 
All  of  these  are  elements  which  might  cause  displacement  of  the 
developing  cuspids.  Should  the  advance  of  eruption  not  keep  pace 
with  the  development  of  the  alveolar  bone,  imprisonment  is  likely; 

1  Possibly  resorbed  or  decalcified  instead  of  carious.     (Editor.) 


IMPACTION  OF  TEETH 


289 


Fig.  264 


again,  the  dense  bone  immediately  about  the  first  bicuspid  and 
lateral  incisor  may  offer  a  deflecting  resistance.     Examining  the 

texture  of  the  bone  about  these 
parts,  it  is  evident  that  the 
direction  of  least  resistance  to 
the  advance  of  a  much  deflected 
crown   is   into  the    cancellated 

Fig.  265 


Upper  jaw,  with  the  third  molar  directed 
forward  and  impinging  upon  the  second 
molar.  The  small  tooth  situated  high  up 
in  the  anterior  part  of  the  jaw  was  forced 
there  by  the  spade  of  the  grave-digger. 
The  artist's  accuracy  in  delineating  all 
parts  of  the  specimen  has  rendered  this 
explanation  necessary.     (Tomes.) 


A  second  molar  of  the  upper  jaw, 
with  the  wisdom  tooth  inverted  and 
embraced  within  the  roots.      (Tomes.) 


bone  of  the  incisor  portion  of  the  alveolar  process;  hence  it  is  most 
usual  to  flnd  the  crowns  of  these  teeth  lying  with  their  cusps 
pointing  forward  (Fig.  266).     Several  recorded  cases  have  the  posi- 


FiG.  266 


Abnormal  jaw,  showing  impacted  cuspids.      (Cryer.) 


tions  shown ;  one  or  both  of  the  teeth  may  be  impacted.    Cuspid  teeth 
may  erupt  into  the  nasal  cavity  or  appear  in  the  canine  fossa,  and  pre- 
19 


290     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

sent  the  crowns  cheekwise,  or  lie  horizontally  and  above  the  roots  of 
the  bicuspids. 

Fig.  267 


Impacted  bicuspid.     (Salter.) 

Glas,  of  Vienna,  discovered  a  cuspid  in  the  nasal  floor  associated 
with  calcic  formations  in  its  ulcerated  surface  (rhinolith).  The 
patient,  aged  nineteen  years,  had  frequent  fetid  eructations,  with 
vomiting  of  green,  foul-smelling  masses.  With  the  removal  of  the 
cuspid  the  vomiting,  etc.,  ceased. 

Fjg.  268 


Lower  maxilla,  in  which  the  right  second  bicuspid  is  placed  obliquely,  the  root  being 
directed  backward.  The  crown,  though  exposed,  does  not  rise  above  the  level  ot  the 
alveolar  margin.      (Tomes.) 

Impaction  of  Other  Teeth. — While  impactions  are  most  common  in 
connection  with  the  teeth  named,  any  other  teeth  of  a  denture  may 


IMPACTION  OF  TEETH 


291 


be  imprisoned.     Fig.  267  shows  an  impacted  bicuspid  whose  root 
development  has  been  normal  as  regards  its  length,  but  whose  curve 


Fig.  269 


Imprisoned  central  incisor.      (Kirk  and  Cryer.) 

has  been  modified  by  the  resistance  of  surrounding  tissues.  Fig.  269 
exhibits  an  imprisoned  central  incisor,  whose  retention  was,  no 
doubt,  determined  and  malposition  caused  by  the  development  and 
presence  of  the  brood  of  supernumerary  teeth  which  surrounded  its 
crown.  • 

Fig.  270 


Maxilla,  in  which  the  temporary  cuspids  (the  sockets  of  which  are  shown  by  the 
dotted  lines)  were  retained,  and  the  permanent  canines  developed  within  the  substance 
of  the  jaw.  The  bone  has  been  removed  on  the  one  side  to  show  the  direction  taken 
by  the  tooth,  which  has  been  twisted  on  its  axis  to  the  extent  of  a  quarter  of  a  turn 
(Tomes.) 


Upper  incisor  teeth  have  been  seen  inverted  and  their  crowns 
erupted  into  the  nasal  cavity,  where  they  have  produced  inflammation, 


292     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

which  later  became  infective.^  A  supernumerary  tooth  has  been 
found  in  the  floor  of  the  nasal  cavity^  so  that  presence  of  all  normal 
teeth  should  not  exclude  extra  teeth  from  consideration  in  making 
a  diagnosis.  Skiagraphy  may  demonstrate  an  unsuspected  super- 
numerary. 

Impacted  teeth  do  not  necessarily  produce  such  pathological  con- 
ditions as  produce  untoward  symptoms.     The  malposition  of  the 
impacted  teeth  either  in  total  or  partial  impaction  may,  however, 
lead  to  malposition  of  other  teeth,  or  results 
Fig.  271  such  as    caries.    The  relation  of  impacted 

teeth  and  any  ulterior  disease  condition  is 
settled  by  the  facts,  the  probabilities  of 
relation,  or  the  results  of  their  removal. 

Symptoms. — The  most  common  symptom 
attendant  upon  impaction  of  teeth,  judging 
from  the  obtainable  records  of  cases,  is  tri- 
b;°"r4tr''p3i:;'  fe<^ial  neuralgia  of  any  degree,  caused  .by 
(Cryer.)  impingement  of   the  malposed  tooth    upon 

nerve  filaments  or  trunks.  Cryer^  records  a 
case  where  a  supramaxillary  neuralgia  was  traced  to  the  presence  of  a 
central  and  lateral  incisor,  and  a  cuspid  tooth  in  the  anterior  wall 
of  the  antrum;  they  were  only  discovered  by  an  exploratory  opera- 
tion.   A  cure  of  the  neuralgia  was  effected  by  their  removal. 

Impacted  third  molars  frequently  give  rise  to  heavy  rheumatic 
pains  about  the  side  of  the  face  and  jaws,  and  no  doubt  in  such  cases 
as  depicted  in  Fig.  256  would  cause  intractable  and  diffuse  maxillary 
neuralgia.  Salter^  records  a  case  of  long  standing  and  intractable 
neuralgia,  exhibiting  a  constant  painful  area  upon  the  scalp,  and  in 
which  heat  and  tenderness  were  noticed  over  a  swelling  upon  the 
hard  palate.  Immediate  and  permanent  cessation  of  the  neuralgia 
followed  removal  of  the  teeth. 

Dr.  N.  T.  Shields^  describes  a  case  of  great  pain  in  the  region  of 
the  mental  foramen,  accompanied  by  a  later  appearance  of  fever, 
reaching  103.8°,  with  subsequent  enlargement  of  the  submaxillary 
gland,  as  cured  by  the  surgical  removal  of  the  two  impacted  bicuspids 
and  deciduous  tooth  shown  in  Fig.  272. 

Symptoms  of  maxillary  periostitis — heavy,  gnawing,  and  dull, 
throbbing  pain,  with  more  or  less  heat  and  engorgement  of  tissues — 
are  noted  as  an  accompaniment  of  impacted  teeth.    Such  symptoms 

1  Jameson:  International  Dental  Journal,  1899. 

2  Boral:  See  Cosmos,  December,  1911. 

3  Dental  Cosmos,  1896. 

^  Dental  Pathology  and  Surgery. 
5  Dental  Cosmos,  1908. 


IMPACTION  OF  TEETH 


293 


may  herald  the  appearance  of  the  tip  of  the  tooth  through  its  bony 
covering  and  gum. 

Cases  of  maxillary  abscess,  in  the  absence  of  their  usual  cause 
(gangrenous  pulp),  may  run  a  prolonged  and  painful  course,^  involv- 
ing neighboring  structures,  which  may  be  vital,  and  after  free  venting 
be  found  to  have  arisen  about  an  impacted  tooth.     The  probable 

Fig.  272 


Skiagraph    showing   impacted    teeth.      (Shields.) 


explanation  for  many  cases  is  the  partial  absorption  of  the  overlying 
tissues,  permitting  ingress  of  bacteria,  but  in  some  cases  crown 
resorption  may  cause  irritation,  and  bacteria  in  the  blood  may 
localize.  A  few  cases  of  pulp  exposure  have  been  seen  when  a  sinus 
allowed  ingress  of  bacteria  and  the  production  of  caries.     In  such 

1  See  Garretson's  Oral  Surgery  and  Salter's  Dental  Pathology. 


294      MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

case  a  pulp  may  die,  undergo  putresence,  and  cause  apical  abscess 
with  its  symptoms. 

Occasionally  a  circumscribed  swelling  is  noted  upon  some  aspect 
of  a  jaw,  most  frequently  upon  the  palatal  portion  of  the  superior 
maxilla,  which  is  attended  by  inflammatory  symptoms,  and  an 
incision  reveals  an  impacted  tooth.  If  a  plate  has  been  worn,  the 
tissue  between,  and  even  the  bone  may  become  necrotic. 


Fig.  273 


Fig.  274 


X-ray  photograph,  showing  mal- 
posed  cuspid  entirely  embedded  in  the 
bone  and  pressing  upon  the  central. 


Impacted   cuspid  revealed  by  resorption 
of  the  overlying  tissues.      (Burchard.) 


Quickly  forming  cysts  of  the  jaw,  upon  receiving  surgical  treat- 
ment, may  be  found  to  contain  the  crown  of  an  entire  tooth,  this 
evidently  being  the  centre  of  irritation  from  which  the  cystic  forma- 
tion had  its  origin.  Melancholia,  mania,  and  dementia  precox  have 
been  relieved  by  the  extraction  of  impacted  teeth  diagnosticated 
by  skiagraphy.^  This  shows  a  relation  between  cause  and  effect 
(Figs.  275,  276,  277).  M.  C.  Smith^  reports  a  case  of  lifelong 
attacks  of  prostrating  sick  headache  due  to  impaction  of  a  third 
lower  molar  and  relieved  by  its  extraction. 

The  pulps  of  other  teeth  have  been  devitalized  by  the  strangula- 
tion due  to  the  pressure  of  the  crown  of  the  impacted  tooth  upon 
the  apical  tissue,  and  the  production  of  pulp  nodules  in  other 
teeth  through  a  reflex  hyperemia  has  been  noted.  The  resorption 
of  roots  of  other  teeth  has  been  produced  by  the  pressure  of  the 
impacted  tooth. 

Hypercementosis  and  concrescence  have  also  been  produced  by 
the  descent  of  the  tooth  and  have  produced  impaction. 


1  Upson:  Dental  Cosmos,  1910,  p.  527. 

2  Dental  Brief,  1912. 


IMPACTION  OF  TEETH  295 

Resorption  of  the  roots  of  the  impacted  teeth,  or  resorption  of  the 
enamel  and  dentin  of  the  crown  may  occur.  In  one  case,  a  calculus 
in  nowise  associated  with  the  oral  cavity,  and  divided  from  it  by  an 
area  of  pericemental  tissue  was  found.  (See  Resorption  of  Enamel, 
for  illustration.) 

In  all  these  cases  diagnostic  features  exist,  though  none  are  com- 
parable to  the  .T-rays. 

Diagnosis. — The  first  point  of  observance  in  cases  of  suspected 
tooth  impaction  or  of  obscure  supernumerary  teeth  is  an  examina- 
tion of  the  dental  arches.  Are  all  of  the  permanent  teeth  in  position? 
Given  the  absence  of,  for  example,  a  lower  third  molar  from  the 
dental  arch,  with  a  history  of  no  eruption,  and  a  persistent  neural- 
gia, particularly  if  occasionally  accompanied  by  or  alternated  with 
heavy  rheumatic,  or  what  are  known  as  bone  pains,  and  finding  no 
other  evident  cause  of  the  neuralgia,  an  impacted  tooth  would  be 
naturally  inferred  to  be  the  source  of  the  disturbance.  Impacted 
teeth  which  lie  horizontally,  or  nearly  so,  along  the  palatal  vault 
frequently  cause  a  swelling.  This,  taken  in  conjunction  with  the 
absence  of  a  tooth  from  the  dental  arch,  points  to  a  diagnosis  of 
impaction. 

In  very  many  cases  of  impaction,  diagnosis  has  been  a  mere  acci- 
dent; discovery  being  made  in  the  course  of  an  exploratory  surgical 
operation.  In  other  cases  dental  disturbance  has  been  simply  an 
inference,  until  skiagraphy  has  determined  an  impacted  tooth  or 
some  other  lesion  to  be  present.  B.  H.  Catching^  was. the  first 
to  practically  appty  this  diagnostic  test  in  this  connection.  The 
left  upper  central  incisor  of  a  female,  aged  nineteen  years,  became 
loosened,  and  an  exploration  through  its  pulp  chamber  revealed 
a  hard  body  occupying  a  position  part  way  up  the  root,  which  had 
undergone  resorption  to  that  point.  The  cuspid  of  the  left  side  was 
absent  from  the  arch.  A  skiagraph  of  the  parts  (Fig.  273)  revealed 
the  missing  cuspid,  whose  crown  had  impinged  upon  and  caused 
resorption  of  the  central  incisor. 

Impacted  teeth  may  become  uncovered  at  some  aspect  late  in 
life,  and  the  condition  be  discovered  incidentally.  Cases  are  recorded 
where  the  pressure  of  a  plate  has  caused  the  resorption  of  tissues 
overlying  an  impacted  tooth,  thus  revealing  its  presence.  Fig.  274 
illustrates  a  case  w^here  the  presence  of  an  impacted  cuspid  was 
revealed  at  the  age  of  seventy  years,  through  resorption  of  the 
alveolar  bone  and  the  gum  tissue  covering  the  tooth. 

As  the  smooth  feel  of  enamel  is  a  diagnostic  feature  when  instru- 

'  Catching's  Compend,  1896. 


296     MALFORMATIONS  AND  MALPOSITIONS  OF  THE  TEETH 

mental  examination  is  made,  it  is  to  be  remembered  that  the  enamel 
and  dentin  of  an  impacted  tooth  may  undergo  a  true  resorption 
with  the  characteristic  Howship's  lacunse.  When  partly  exposed 
to  the  oral  fluid,  caries  may  occur.  Both  these  conditions  produce 
rough  surfaces,  but  enamel  may  usually  be  felt  at  some  point. 


Fig.   275 


Fig.  276 


Impacted   lower  third  molar;    cause  of 
neuralgia.      (Skiagraph  by  Lodge.) 


Cuspid  tooth,  unsuspected  by  patient ; 
demonstrated  to  have  been  responsible 
for  severe  neuralgias.  Patient,  a 
draughtsman,  had  not  been  able  to 
work  at  his  business  for  the  six  months 
previous.  The  tooth  was  not  known 
to  be  present,  until  revealed  by  a;-rays. 
It  was  removed  from  the  lingual  side. 
(Skiagraph  by  Lodge.) 


Fig.  277 


Impaction  of  upper  third  molar,  without  local  pain,  cause  of  profound  delusions  and 

melancholia.    (Upson. i) 

Treatment. — ^The  treatment  of  cases  of  impaction  is  the  removal  of 
the  offending  tooth.  Whether  or  not  this  comes  within  the  province 
of  the  dental  operator  depends  upon  the  position  of  the  tooth,  and, 
incidentally,  upon  the  usual  range  of  practice  of  that  particular 
practitioner.  When  the  tooth  is  embedded  deeply  in  the  substance 
of  the  jaw,  access  to  it  involves  the  anesthetization  of  the  patient, 


Insanity  Caused  by  Painless  Dental  Disease,  Dental  Cosmos,  1910. 


IMPACTION  OF  TEETH  297 

and  the  removal  of  the  bone  which  obstructs  the  path  of  extraction; 
this  may  be  an  operation  of  some  magnitude,  and  is  usually  done  by 
a  special  surgical  practitioner.  When,  however,  it  is  evident  that 
the  obstructions  to  the  removal  of  the  tooth  consist  of  the  soft 
tissues  and  but  a  lamina  of  bone,  the  operation  for  removal  is  clearly 
within  the  province  of  the  dental  operator.  For  example,  the  pres- 
ence of  an  impacted  cuspid  is  determined,  lying  horizontally  along 
the  lateral  aspect  of  the  roof  of  the  mouth.  The  parts  may  be 
injected  with  a  local  anesthetic  solution,  and  a  cut  made  with  a 
sharp  bistoury  through  the  soft  tissues  from  the  outside  of  the 
swelling,  to  the  bone.  The  flap  thus  outlined  is  raised  from  the 
bone,  the  flap  including  the  periosteum.  A  large,  sharp  bur  is  then 
employed  to  remove  the  covering  bone.  When  the  tooth  is  freely 
exposed  it  may  be  dislodged  with  forceps  or  elevator.  The  parts 
are  then  washed  with  a  hydrogen-dioxid  solution,  dried,  the  flap 
pressed  back  into  place,  and  steresoP  painted  over  the  parts,  or 
a  stitch  or  two  may  be  taken  before  application  of  the  steresol. 
The  mouth  should  of  course  be  kept  as  aseptic  as  possible  both  before 
and  after  operation.    A  simple  clot  kept  aseptic  may  be  sufficient. 

I^ — Purified  gum  lac §ix 

Purified  gum  benzoin -Si 

Balsam  of  tolu 54 

Oil  of  cinnamon  (Chinese) ■     ■  B:s^ 

Carbolic  acid giij 

Saccharin gJ- 

Alcohol Oi.i — M. 

1  Dental  Cosmos,  1S95. 


'       SECTION  III. 

AFFECTIONS   OF    THE  ENAMEL   AND   DENTIN. 


CHAPTER   IX. 
ABRASION,  EROSION,  AND  MECHANICAL  INJURY. 

Formed  by  the  ameloblasts,  which  are  later  changed  into  Nasmyth's 
membrane,  and  borne  upward  with  the  crown  during  the  process 
of  eruption,  enamel  has  no  postemptive  source  of  nutritive  supply 
from  without. 

Its  only  conjectural  source  of  nutrition  is,  therefore,  from  the 
pulp  via  the  dentinal  tubuli.  This  seems  to  have  been  proved  by 
Caush,  and  later  by  others.  (See  p.  173.)  Teeth  do  change  in  color 
with  advancing  age,  generally  becoming  yellower;  this  is  probably 
due  to  tubular  calcification  (which  see),  rendered  possible  by  the 
tubes  containing  organic  matter  which  are  now  supposed  to  permit 
a  slow  interchange  of  nutritive  sap.^  This  coloration  may  be  seen 
in  cases  of  abrasion  and  in  some  cases  extends  even  into  the  second- 
ary dentin  associated.  The  editor  has  a  patient  with  a  vital  tooth 
of  mahogany  brown  color,  which  she  claims  changes  the  depth  of 
color.  Changes  in  the  color  of  the  dentin  may  be  transmitted 
through  enamel,  which  is  normally  almost  or  even  quite  transparent. 
Such  a  transparency  may'  be  seen  at  the  incisal  edges  of  thin  incisors 
before  these  edges  are  worn  down.  Another  proof  of  transmission 
of  color  through  enamel  is  seen  in  caries;  a  bluish-black  or  white 
appearance  is  caused  by  the  decayed  mass  or  decalcified  inner  surface 
of  the  enamel. 

Again,  amalgam  or  gold,  oxyphosphate  or  oxychlorid,  reflects  its 
color  through  enamel,  and,  in  excavating,  the  shadow  of  the  excavator 
may  be  seen  through  thin  walls.  Enamel  may  be  stained  or  whitened 
by  decalcification  due  to  causes  acting  externally.    Extreme  polishing 

1  C.  Francis  Boedecker:  Dental  Cosmos,  September,  1911. 

(299) 


300  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

may  also  cause  a  new  character  of  light  reflection,  simulating  a  change 
in  color.  Talbot  claims  a  change  in  color  of  teeth  during  prolonged 
illness,  such  as  pneumonia,  typhoid  fever,  syphilis,  tuberculosis,  and 
in  pregnancy.^  With  advancing  age,  the  translucency  of  teeth 
verges  more  toward  transparency — apparently  a  sclerotic  change 
in  the  dentin.     (See  Transparency.) 

After  implantation,  a  tooth  may  somewhat  change  its  color,  but 
this  evidently  cannot  be  due  to  nutrition  from  the  pulp,  as  this 
organ  will  have  been  removed  before  implantation.  It  would  seem 
that  it  may  take  up  coloring  matter  from  the  saliva. 

Enamel  may  suffer  mechanical  and  chemical  injury,  but  whether 
it  may  undergo  constructive  changes  or  retrograde  metamorphosis 
is  at  present  only  conjectural.  There  is,  however,  a  possibility 
that  a  molecular  change  may  occur  as  a  result  of  slow  interchange 
of  fluid,  environment,  or  impact  of  mastication. 

The  dentin  and  cementum  contain  about  28  and  30  per  cent,  of 
organic  matter,  respectively,  and  stain  deeply  and  permanently  with 
great  readiness. 

Possessed  of  living  cells,  they  also  undergo  changes  in  their  structure 
under  the  influence  of  various  stimuli,  their  substance  being  added 
to  or  reduced  according  to  circumstances.  They  are  also  acted  upon 
by  mechanical  and  chemical  agencies,  if  exposed  to  their  influence. 

ABRASION. 

Abrasion  is  the  mechanical  wearing  away  of  tooth  substance. 

Occurrence. — It  occurs  most  commonly  upon  the  occlusal  surfaces 
of  teeth,  but  is  also  found  upon  the  approximal  and  labial  surfaces, 
the  labial  cervix,  and  more  rarely  upon  the  lingual  surfaces.  It  is 
also  seen  in  the  temporary  denture,  especially  in  the  molars,  and 
is  found  in  animals  (Figs.  288  and  289). 

'  Appearance. — Purely  abraded  surfaces  present  a  smooth,  flat,  or 
concaved,  highly  polished  appearance.  The  surface  may  become 
stained  or  otherwise  altered  in  color,  or  subsequent  caries  may 
remove  its  smooth  surface. 

Occlusal  Abrasion. — Occlusal  wear  is  very  common,  and  occurs 
largely  with  men  who  chew  tobacco;  the  contained  silex,  being  gritty, 
acts  as  an  abrasive.  Such  wear,  due  to  the  use  of  hard  food  or  gritty 
substances,  is  seen  in  skulls  of  aboriginal  man.  Ottofy  describes  a 
peculiar  form  of  wasting  due  to  chewing  betel  nut  mixed  with  bay 
leaves  and  slaked  lime.      No  doubt  a  gritty  element  is  introduced. 

»  Dental  Cosmos,  1905,  p.  29. 


ABRASION 


301 


Some  degree  of  occlusal  wear  is  accepted  as  normal  to  all  teeth,  the 
act  of  mastication  producing  marks  or  facets  at  the  point  of  articu- 
lation of  antagonizing  teeth.  A  tip-to-tip  variety  of  occlusion 
permits  free  lateral  movement  of  the  lower  jaw,  and  a  herbivorous 
type  of  articulation  causing  abrasion.  It  is  also  frequent  in  those 
cases  presenting  the  first  degree  of  prognathism.  In  some  of  these 
cases,  the  labial  surfaces  of  the  upper  incisors  and  cuspids,  and  the 
linguo-incisal  margins  of  the  lower  incisors  are  worn.  A  single  over- 
lapped lower  tooth  may  abrade  an  upper  tooth  in  this  manner. 

The  gritting  of  teeth  is  also  a  cause.  This  gritting,  termed  "bruxo- 
mania,"  may  occur  only  at  night  or  for  a  few  minutes  each  day; 
again  it  may  appear  for  entire  days,  weeks,  and  months,  not  ceasing 
even  during  sleep.  In  such  cases  the  teeth  are  worn  down  flat. 
Maria  and  Pietkiewiczi  noted  12  cases  of  central  nervous  lesions, 
mostly  dementia,  developing  bruxomania;  also  it  has  been  noted  in 
cases  of  epilepsy  and  chorea. 

A  clay  pipestem  may  wear  a  hole  of  its  own  diameter  in  the  incisal 
edges  of  anterior  teeth;  other  stems  wear  less.  Upholsterers  and 
seamstresses  have  peculiar  abrasions  (tack  holding,  thread  biting). 

Fig.  278 


Abrasion  of  anterior  teeth,  with  loss  of  posterior  occlusion.     (W.  A.  Capon.) 

The  undue  loss  of  posterior  occlusion  and  consequent  overuse  of 
the  anterior  teeth  cause  their  abrasion  after  the  manner  shown  in 
Fig.  278.  A  marked  overbite,  produced  in  any  manner,  may  cause 
lingual  abrasion  of  upper  anterior  teeth. 

Where  the  abrasion  occurs  in  a  fairly  regular  manner,  four  degrees 

of  abrasion  are  classified:     (1)  Abrasion  removing  the  cusps;   (2) 

abrasion  removing  the  occlusal  third  of  the  crown;   (3)   abrasion 

removing  the  middle  third  of  the  crown;  (4)  abrasion  extending  to 

•  the  gum  line  or  beyond.    (Broca.)     (See  Figs.  279  and  280.) 

When  there  is  a  marked  overbite  occlusion,  with  a  consequent 
lessening  of  the  lateral  movement  of  the  mandible,  the  teeth  do 


1  Dental  Cosmos,  1907,  p.  525. 


302  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

not  acquire  flattened  contact  surfaces,  but  their  cusps  increase  in 
sharpness  and  pointedness.  This  at  times  becomes  exaggerated,  and 
produces  an  interlocking  of  cusps  or  rather  worn  surfaces  which 
have  very  sharp  edges. 

Fig.  279 


The  first  and  second  degrees  of  abrasion.     Specimens  from  museum  of  Philadelphia 

Dental  College. 

Fig.  280 


The  third  and  fourth  degrees  of  abrasion.    Secondary  dentin  plainly  visible.    Specimens 
from  museum  of  Philadelphia  Dental  College.  , 

In  the  first  degree  of  abrasion,  the  dentin  is  often  hollowed  out  in 
advance  of  the  enamel  of  the  cusps,  forming  concave  places  in  which 


ABRASION  303 

berry  seeds  lodge  and  cause  annoyance.  These  spots  are  at  times 
hypersensitive.  The  plane  surfaces  also  are  often  sensitive  upon 
merely  rubbing  the  teeth  together. 

Labial  and  Approximal  Abrasions. — Some  forms  of  abrasion  have 
been  attributed  to  too  vigorous  use  of  tooth-brushes,  particularly 
when  gritty  powders  are  employed.  There  is  no  doubt  that  mechan- 
ical abrasion  about  the  necks  of  teeth  is  produced  in  this  manner,  the 
gum  line  receding  beyond  the  enamel  border,  exposing  the  cementum; 
and  a  careful  examination  will  reveal  the  cementum  and  next  the 
underlying  dentin  to  be  affected;  the  enamel,  when  abraded,  shows 
first  as  a  facet,  then  as  a  spot  of  bare  dentin  with  thin  edges  of  enamel 
around  it  (see  the  left  lateral  in  Fig.  299),  and  later  the  area  may  be 
grooved.  As  a  rule,  however,  the  effect  shown  in  Fig.  298,  lower 
jaw,  is  the  more  common.     These  tooth-brush  abrasions  are  quite 

Fig.  281 


Abrasion  due  to  employment  for  twenty  years  of  a  gritty  English  tooth  paste. 
At  7,  gold  crown  abraded.     (Miller.) 


characteristic.  In  well-kept  dentures,  the  gums  are  seen  to  have 
receded  from  their  normal  line,  but  may  exhibit  little  evidences  of 
turgescence;  the  roots  of  the  teeth,  upper  and  lower,  are  exposed  to 
a  greater  or  less  extent  along  their  labial  and  buccal,  but  not  usually 
along  their  lingual  aspects;  and  they  are  excavated  to  variable 
depths,  upon  the  bicuspids  and  first  molars  more  than  upon  the 
other  teeth,  as  here  the  greatest  force  of  brushing  is  received.  The 
depressions  have  a  normal  dentin  color,  sometimes  deepened  in  the 
mouths  of  non-smokers,  and  which  in  smokers  may  be  periodically 
blackened  by  deposits  of  carbon.  If  caries  supervene,  the  abraded 
areas  lose  their  normal  color,  and  may  be  readily  indented  by  sharp 
instruments,  which  they  resist  before  the  advent  of  caries.  The 
bicuspids  and  molars,  particularly,  may  be  grooved  in  such  manner 
as  to  require  restoration  by  fillings. 


304 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

Fig.  282 


Photomicrograph  of  sediment  obtained  by  washing  tooth  paste,   which  caused   the 
abrasion  shown  in  Fig.  281.     (Miller.) 


Fig.  283 


A     B 


Abrasion  of  lingual  surface  by  assiduous  brushing  with  tooth  powder.     At  D  and  E 
amalgam  worn  down.  (Miller.) 


ABRASION 


305 


Miller^  investigated  this  subject  very  carefully,  and  found  that 
the  grit  in  many  forms  of  tooth  powder,  vigorously  used,  was  quite 


Fig.  284 


Artificial  abrasion  produced  by  brushing  with  a  much-used  English  tooth  paste  with 
motor  brush  for  eighteen  hours.    Remains  of  gold  filling  in  first  bicuspid.    (Miller.) 

Fig.  2=':5 


Gradual  wear  of  both  tooth  substance  and  filling  material,  notwithstanding  the  open 

bite.     (Miller.) 


competent  to  wear  away  tooth  structure,  gold,  and  other  fillings 
(Figs.   281  to  284).     Figs.  283  and  286  show  a  lingual  wasting, 

1  Dental  Cosmos,  1907. 
20 


306  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

resembling  graphic  erosion.  In  both  cases  abrasion  is  proved  by 
the  wasting  of  metal,  which  acids  could  hardly  accomplish.  Miller 
experimentally  proved  abrasion  competent  to  produce  the  grooves 
known  as  "wedge-shaped  defect"  (Figs.  284  and  298). 

Calculus  may  be  worn  in  like  manner,  either  by  the  brush  or  by 
the  festoon  of  a  plate  (Fig.  287). 

Miller  found  that  among  clinic  patients  who  never  used  a  tooth- 
brush the  labial  abrasion  was  wanting,  and  he  observed  that  a 
cessation  of  wear  followed  the  abandonment  of  the  use  of  gritty 
powder  and  the  adoption  of  a  soft  brush  and  mild  powder,  which  is 
the  evident  indication  in  such  a  case. 

A  clasp  may  abrade  a  tooth,  and,  if  food  debris  be  retained  on  its 
inner  side,  caries  may  follow  in  the  abraded  area.  The  purely  abraded 
surface  will  be  polished.  Slight  approximal  abrasion  may  be  normal 
as  a  facet,  due  to  the  rubbing  of  one  tooth  upon  another  at  the 
contact  point.  A  marked  example  of  this  was  seen  in  the  mandible 
of  a  skull  of  a  Maori.    (Museum  of  Philadelphia  Dental  College.) 

The  third  lower  molars  are  locked  beneath  the  distal  surface  of 
the  crowns  of  the  second  molars.  Some  form  of  bone  loss  occurred, 
producing  looseness  of  the  third  molars.  The  individual  motion  of 
the  teeth  produced  a  deep  abrasion  of  the  enamel  of  the  second 
molars  upon  the  distal  surface,  and  an  occlusoproximal  abrasion  of 
the  third  molars.     (Also  see  Fig.  338.) 

Grit  in  powder  may  easily  be  detected  by  taking  a  small  portion 
between  the  incisor  teeth,  or  may  be  found  by  elutriating  the 
powder,  i.  e.,  place  in  water,  stir,  let  settle  for  a  few  seconds,  pour 
off  the  supernatant  fluid,  and  examine  the  sediment  as  above,  or 
microscopically  (Fig.  282). 

Miller  found  from  experiments,  as  to  the  effects  of  various  acids 
acting  for  a  time  and  followed  by  brushing  with  abrasives,  that  it 
depends  very  materially  upon  the  nature  of  the  acid.  Those  acids 
which  rapidly  decalcify  (soften)  the  dentin,  of  which  we  may  take 
hydrochloric  and  lactic  as  types,  most  readily  retard  the  wearing 
awa}^  by  friction  (unless  the  friction  be  so  great  as  to  wear  in  spite 
of  the  decalcification).  While  those  which  act  slowly  on  the  dentin 
(oxalic,  tartaric,  etc.),  as  well  as  those  which  have  a  macerating 
effect  on  decalcified  dentin,  may  be  wanting  in  this  influence.  He 
concluded  that  wear  could  not  be  produced  by  acid  alone,  but  that 
any  acid  or  acid  salt  which  possesses  the  power  of  extracting  the 
calcium  salts  from  enamel,  or  of  breaking  up  the  connection  between 
the  enamel  prisms,  may  accelerate  the  process  of  wasting,  provided 
the  necessary  mechanical  factor  works  together  with  it.  Miller 
found  food  to  be  a  negligible  quantity  as  to  wear  upon  labial  surfaces. 


ABRASION  307 

The  editor  has  a  patient  presenting  the  general  characteristics  of 
Fig.  300,  who  has  been  a  brush  enthusiast,  and  was  taught  in  early 
life  to  use  a  toilet  soap  containing  fine  pumice  (Bazin's  poncine  soap). 

Extensive  approximal  abrasion  may  be  due  to  extrusive  elonga- 
tion of  a  tooth  in  one  or  both  jaws,  causing  a  tooth  to  occlude  with 
its  antagonist  with  a  glancing  motion. 

In  this  manner,  specimens  are  produced  abraded  from  the  occluso- 
approximal  angle  to  nearly  the  apex  of  the  root. 

The  festoon  of  a  metal  plate  may  rapidly  cause  abrasion  of  the 
lingual  cervix  of  a  tooth.  The  condition  is,  however,  rare;  caries 
being  more  common.  In  the  editor's  practice  a  case  was  seen,  in 
which  several  teeth  were  so  affected  in  a  few  months,  by  an  ill-fitting 
metal  plate.  The  festoon  of  a  vulcanite  plate  has  also  produced 
such  an  abrasion. 

Abrasion  sometimes  follows  caries,  when  the  latter  has  become 
freely  exposed  to  attrition.  The  softened  surface  wears  away  and 
the  part  assumes  a  polished  appearance,  but  is  discolored  as  the 
result  of  the  stain  due  to  the  caries.  (There  is  also  eburnation, 
which  see.) 

It  is  probable  that  a  hyperacid  condition  of  the  saliva  in  con- 
nection with  mechanical  forces  may  be  a  cause  of  rapid  abrasion. 
(See  Erosion.) 

Effects  of  Abrasion. — These  are  external  and  internal,  and  most 
marked  in  the  occlusal  variety.  The  crown  wears  down  until  at  times 
the  gum  is  reached.  In  the  process  sharp  edges  of  enamel  are  formed. 
These  splinter  off,  leaving  rough  edges,  or  the  enamel  may  fracture 
or  split  longitudinally,  following  the  axis  of  the  crown.  Supported 
by  dentin  it  does  not  further  break  away  (Fig.  308). 

Sharp  enamel  edges  may  irritate  the  tongue,  producing  ulcers  of  a 
sometimes  chronic  type,  which  acquire  indurated  edges  and  simu- 
late syphilitic  sores  or  epithelioma.  The  causal  relationship  between 
sharp  edges  of  the  teeth  and  lingual  epithelioma  appears  to  be  quite 
clear  in  some  cases.  Brown^  mentions  a  case  of  tetanic  spasms  of 
masticatory  muscles  due  to  this  source. 

Sores  which  have  given  evidence  of  malignancy  and  been  diagnos- 
ticated as  malignant  growths,  have  been  cured  by  rounding  and 
polishing  sharp  and  irritating  enamel  edges  of  teeth. 

The  continued  stimulation  of  the  ends  of  the  dentinal  fibrillse,  which 
are  exposed  in  abrasion,  causes  them  either  to  become  hypersensitive 
or  stimulates  them  to  formative  activity.  Tubule  material  is  built 
upon  the  inner  walls  of  the  tubule,  obliterating  their  lumen.     This 

1  Dental  Cosmos,  1908,  p.  4. 


308  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

Fig.  286  Fig.  287 


a,  abrasion  of  lingual  surfaces;  h,  of 
amalgam  filling  produced  by  a  plate. 
(Miller.) 


Abrasion  of  calculus.  (Miller.) 


Fig.  288 


Fig.  289 


Abrasion  of  lower  incisors  of  a  horse     Defects    resembling  wasting    in    the   teeth 
produced  by  "  cribbing. "     (Miller,  after  of  a  sea  lion.     (Miller,  after  Murie.) 

Kitt.) 


ABRASION  300 

is  the  so-called  tubular  consolidation  or  calcification  (eburnation). 
Accompanying  this,  secondary  dentin  is  often  formed.  As  a  result, 
most  commonly  the  pulp  chamber  of  the  crown  is  filled  up  with 
secondary  dentin  as  the  abrasion  proceeds,  and  the  crown  may  often 
be  worn  off  until  the  cervix  is  reached,  while  the  pulp  remains  vital 
and  covered  (Fig.  280).  In  some  cases  the  abrasion  closely  ap- 
proaches the  pulp,  which  has  failed  to  protect  itself,  probably  because 
of  atrophy  of  odontoblasts,  and  the  phenomena  of  hyperemia,  or 
even  exposure,  and  its  results  occur.  A  left  upper  bicuspid  of  the 
second  skull  in  Fig.  280  was  in  this  state. 

The  causes  and  phenomena  of  abrasion  of  the  temporary  teeth  are 
practically  the  same  as  in  the  case  of  adults,  except,  perhaps,  that 
children  are  more  subject  to  the  action  of  rectal  parasites,  as  ascaris 
lumbricoides,  tenia,  etc.,  or  suffer  from  irritable  bladder  due  to 
hyperacidity  of  the  urine.  These  conditions  commonly  produce  a 
reflex  stimulation  of  the  muscles  of  mastication,  resulting  in  nocturnal 
gritting  of  the  teeth. 

Fig.  290 


Same  case  as  Fig.   278.     Bite  opened  by  bridge-work,   posteriorly.     Anterior  teeth 
restored  by  means  of  Land  jacket  crowns.     (W.  A.  Capon.) 

Treatment  of  Abrasion. — In  the  cases  of  cupped  occlusal  dentin, 
hard  fillings  of  platinum  gold  or  platinized  gold  inlays  are  best. 
Whether  the  filling  be  built  in  or  an  inlay  be  set,  it  is  advisable  not 
to  cut  too  closely  to  the  enamel  in  making  the  cavity,  for  the  struc- 
ture of  such  a  wall  is  often  fractured  after  filling  when  this  is  done. 
If  possible  the  form  in  Fig.  291,  with  retention  made  elsewhere  than 
near  the  side  enamel  is  preferable.  Inlays  requiring  only  pin 
anchorage  are  preferable  when  undercutting  would  weaken. 

If  nearly  all  teeth  are  present  and  the  abrasion  slight,  bridge-work 
may  be  used  to  restore  the  full  occlusion  without  attempt  at  restora- 
tion of  the  worn  surfaces. 

If  the  abrasion  of  the  upper  anterior  teeth  be  deep,  the  bite  may 
be  raised  by  appropriate  posterior  crowns  or  bridges,  and  solid 
platinum-gold  fillings  may  be  built  upon  the  anterior  teeth,  either 


310 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 


Fig.  291 


the  uppers  alone  or  upon  both  the  upper  and  lower  teeth.  Anchor- 
age may  be  obtained  in  the  dentin,  or  screws  may  be  planted  in  the 
dentin  between  the  enamel  and  pulp  and  the  fillings  be  built  about 
them.    Instead  of  malleted  fillings,  tips  of  the  gold-inlay  type  may 

be  made  (Figs.  292  and  293).  Casting  the 
inlay  is  a  simpler  method.  Usually  it  is 
better  to  use  an  alloy  of  iridioplatinum 
gold.  This  applies  also  to  the  lingual 
occlusal  abrasion  of  incisors. 

For  those  cases  in  the  second  degree, 
as  a  means  of  limiting  the  abrasion,  Dr. 
J.  C.  Curry  has  introduced  small  trun- 
cated cones  of  unannealed  iridioplatinum, 
which  are  to  be  cemented  into  holes 
drilled  into  the  occlusal  faces  of  the  molars 
and  bicuspids  with  an  inlay  drill  of  exactly  corresponding  size, 
mounted  in  the  right-angle  hand  piece.  As  many  are  put  in .  as 
the  safety  of  the  pulp  and  the  enamel  will  permit.  They  act  upon 
the  same  principle  as  steel  nails  in  a  shoe  heel. 


Manner  of  preparing  the 
outer  retaining  wall  of  a 
cavity  in  case  of  cupped  oc- 
clusal abrasion. 


Fig.  292 


Fig.  293 


Fig.  294 


fl\ 


u 


Gold  tip  for  abraded 
teeth  with  living  pulps. 
(Evans.)  If  cast  the  mar- 
gins are  to  be  beveled  out- 
wardly. 


Gold  tip  for  abraded 
teeth  with  pulps  re- 
moved.    (Evans.) 


Porcelain-faced  crowns 
for  teeth  with  living  pulps. 
(Evans.) 


In  other  cases,  after  securing  a  proper  opening  of  the  bite  and 
posterior  occlusion  with  crowns  or  bridges,  single  porcelain-faced 
gold  or  platinum  crowns  may  be  made  to  cover  each  of  the  anterior 
teeth.  For  this  purpose  the  crown  is  appropriately  reduced  to 
convenient  form,  but  the  pulps  need  not  be  destroyed.  Fig.  294 
represents  the  method  outlined  by  Evans. ^  There  can  be  no  objec- 
tion to  pulp  removal  in  any  of  these  cases,  if  for  any  reason  a  dowelled 
crown  seem  preferable. 

1  Crown  and  Bridge  Work. 


ABRASION  •  311 

Land  jacket  crowns,  consisting  of  a  wedge-shaped  platinum  jacket, 
with  a  porcelain  facing  attached  by  means  of  one  of  the  numerous 
inlay  bodies,  may  be  used  instead  of  the  Evans  crown.  In  some  cases 
other  forms  of  crowns  may  be  indicated  (Fig.  290). 

There  present  at  times  cases  of  abrasion  in  which,  aside  from  the 
wear,  pyorrhetic  conditions  may  be  present,  or  where  bridges  cannot 
be  properly  inserted,  especially  when  only  a  few  teeth  remain. 

If  this  pertain  to  the  upper  jaw  only,  the  lower  denture  may  be 
restored  to  usefulness,  the  upper  teeth  extracted,  and  a  full  upper 
denture  inserted;  this  permits  the  adjustment  of  the  bite  to  any 
desired  level.  If  the  conservation  of  a  few  teeth  is  desirable,  they 
may  be  crowned  or  bridged;  the  occlusion  being  raised  if  desirable, 
then  a  plate  constructed.  If  the  condition  be  transferred  to  the 
lower  jaw  and  the  anterior  teeth  be  in  good  condition,  a  piece  with 
the  Roach^  or  Morgan  type  attachment  may  be  fixed  upon  cuspid 
or  bicuspid  crowns. 

It  is  to  be  remembered  that  in  any  case  of  opening  of  the  bite,  the 
occlusion  is  to  be  restored  throughout. 

The  bite  must  not  be  raised  by  means  of  partial  plates  which  strike 
before  the  natural  or  crowned  teeth,  as  they  tend  to  embed  them- 
selves in  the  soft  tissues  and  create  inflammation. 

If  the  bite  be  only  slightly  raised  by  plates,  this  embedding  will 
cause  a  return  to  the  original  condition.  Neither  must  too  great  a 
strain  be  placed  upon  supporting  teeth  (see  Overwork  of  Teeth). 

In  case  of  hypersensitivity,  Robinson's  remedy,  silver  nitrate, 
nitric  acid,  or  the  actual  (hot  burnisher)  or  the  electrocautery  may 
be  effective;  if  not,  the  areas  should  be  excavated  and  filled,  or,  if 
necessary,  the  pulp  should  be  devitalized. 

If  the  abrasion  be  caused  by  tobacco  its  use  should  be  stopped. 
A  difficult  class  of  cases  to  treat  is  found  in  those  highly  nervous 
individuals  who  grit  their  teeth  during  sleep.  It  is  probable  and 
reasonable  that  this  cause  alone  may  serve  to  explain  abrasions  trace- 
able to  no  other  source.  The  cure  of  such  cases  as  these  could  only 
be  possible  through  the  wearing  at  night  of  some  modified  form  of 
interdental  splint.  Arnone  has  described  a  simple  vulcanite  splint 
for  the  lower  teeth,  to  open  the  molars  about  one-sixteenth  of  an 
inch  and  the  incisors  one-half  inch.  This  he  calls  "the  insulator," 
and  is  to  be  vulcanized  at  160°  C.  It  is  to  have  the  upper  surface 
rounded  (Fig.  295).  He  also  describes  "the  paraglossus,"  a  double 
vulcanite  splint  made  in  one  piece  to  be  inserted  by  bruxomaniacs 
during  sleep,   or  by  epileptics  during  the  forewarning   "aura,"  if 

1  Dental  Cosmos,  1908,  p.  17. 


312 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 


present,  to  prevent  grinding  or  tongue  biting.^  The  cases  naturally 
indicate  the  medicinal  use  of  a  bromide  before  retiring,  unless  the 
causes  can  be  discovered  and  removed. 

If  such  gritting  be  present  in  children,  the  evidences  of  irritable 
bladder,  due  to  hyperacidity  of  the  urine,  or  of  rectal  parasites,  should 
be  sought  and  treated.  The  urine  may  be  rendered  alkaline  by  the 
use  of  potassium  salts,  and  kept  so  by  restriction  to  a  largely  vegetable 
diet.  Belladonna  may  be  used  to  reduce  vesical  irritability.  Rectal 
parasites  may  be  removed  by  the  use  of  vermifuges,  or,  occasionally, 
by  rectal  injections. 


Fig.  295 


Fig.  296 


The  "insulator."     (Arnone.) 


The  "  paraglossus. "  The  meta 
groove  shown  relates  to  another 
method  of  construction. 


Fig.  297 


RESORPTION   OF  ENAMEL. 

Definition. — Resorption  of  enamel  is  the  removal  of  enamel  sub- 
stance by  soft  tissue  containing  osteoclasts. 

Occurrence. — It  occurs  externally  only 
in  impacted  teeth  surrounded,  at  least 
in  part,  by  irritated  tissue,  and  internally 
very  rarely  after  resorption  of  dentin  by 
the  pulp2  (Fig.  297).     (See  Pulpitis.) 

Such  tissue  may  also  be  found  in  der- 
moid cysts,  and  causes  the  resorption  of 
teeth.    (See  Fig.  32.) 

Pathology  and  Morbid  Anatomy. — Osteo- 
clasts approximate  the  enamel  as  they  do 
cementum,  decalcify  and  resorb  it.  The 
There  result  irregular  excavations  (How- 
ship's  lacunae)  and  white  or  discolored  areas  of  evident  slight  decal- 
cification of  the  enamel.    A  deposition  of  bone  into  the  area  may 


Impacted  cuspid  with  re- 
sorption of  enamel  and  a 
hematogenic  calculus. 
(Miller.) 

dentin  is  next  attacked. 


1  Dental  Cosmos,  1908,  p.  924. 

2  Hopewell-Smith:  Histology  and  Pathohistology  of  the  Teeth. 


EROSION 


313 


occur.*  The  process  is  probably  the  result  of  a  non-septic  inflam- 
mation, as  in  the  case  of  root  resorption.  (See  Interstitial  Gingivitis 
and  Resorption.) 

The  enamel  may  be  resorbed  from  its  internal  surface  after  the 
resorption  of  dentin  by  the  pulp  (see  Chapter  XVI),  and,  as  shown 
by  Woods,  may  be  filled  in  with  adventitious  material  of  a  structure 
resembling  cementum. 

Treatment. — Should  the  disease  by  chance  occur  upon  a  tooth 
which  later  has  been  drawn  into  place,  the  area  may  be  filled; 
otherwise  it  has  only  a  pathological  interest. 


Fig.  298 


Fig.  299 


Case  described  as  erosion.     (Darby.)  Case  described  as  erosion.   (Darby.) 

Fig.  300 


A  case  of  erosion  (drawn  from  the  cast) :   B,  silhouette  from  a  perpendicular  line  through 
the  left  centrals,  upper  and  lower,  showing  the  loss  of  substance.   (Black.) 


EROSION. 

Definition. — Erosion  of  the  teeth  is  a  term  applied  to  the  chemical 
or  chernicomechanical  destruction  of  the  hard  tissues  of  the  teeth 
in  such  a  manner  that  broad,  shallow,  smooth  excavations  are 
made  in  the  enamel  and  dentin  in  situations  free  from  attrition 
by  mastication. 

"  Hopewell-Smith:  Histology  and  Pathohistology  of  the  Teeth. 


314  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

Figs.  298,  299,  and  300  illustrate  the  characteristic  appearance  of 
areas  until  recently  supposed  to  be  due  to  the  chemical  or  chemico- 
mechanical  solution  which  has  been  termed  erosion. 

The  demonstrations  of  Miller  with  reference  to  abrasion  of  labial 
and  lingual  surfaces  of  teeth  by  means  of  the  tooth-brush  and  gritty 
powders,  and  the  abrasion  of  approximal  surfaces  into  grooves  in 
animals  by  the  drawing  of  gritty  grasses,  etc.,  through  or  along  the 
teeth,  or  the  gnawing  of  bones  by  carnivora,  etc.,  have  cast  a  heavy 
cloud  of  doubt  upon  the  chemical  etiology  of  what  have  been  usually 
considered  as  erosions  due  to  the  action  of  acid  sodium  phosphate 
excreted  by  the  mucous  glands  of  the  lips  or  cheek. 

The  appearance  illustrated  in  Fig.  298,  lower  jaw,  and  in  Figs. 
299  and  300  might  readily,  in  the  light  of  Miller's  demonstrations, 
be  regarded  as  abrasion,  if  the  causes  (brush  and  abrasive  powders) 
he  suggests  be  found;  but  the  graphic  outlines  shown  in  Fig.  298, 
upper  anterior  teeth,  seem  difficult  to  harmonize  with  the  abrasion 
theory.  The  cases  of  this  sort  are  rare  as  compared  with  the  others, 
the  editor  recalling  but  two  having  the  peculiar  undercut  mesial  and 
distal  erosion  borders.  The  spreading  of  brush  bristles,  as  the  brush 
is  brought  from  the  gum  down,  might  account  in  part  for  this,  but 
in  one  of  the  cases  mentioned  there  w^as  also  an  undercut  at  the 
incisal  border,  which  would  render  the  theory  difficult  of  application. 

One  case  was  in  a  man  aged  forty-five  years,  a  German  Jew, 
fond  of  wines,  beer,  etc.,  at  meals;  the  other  a  middle-aged  maiden 
lady  of  nervous  temperament,  with  whitening  hair,  slightly  wrinkled 
skin,  and  some  evidences  of  goutiness. 

According  to  Miller,  acids  or  acid  salts,  which  can  extract  calcium 
salts,  may  accelerate  the  wasting  process  provided  the  necessary 
mechanical  factor  works  with  it  and  wears  off  the  decalcified  tissue 
before  it  becomes  leathery,  when  wear  is  retarded.  Kirk  burnt 
asbestos  cloth,  treated  it  with  hydrochloric  acid,  neutralized  this 
with  ammonia,  washed  it  with  distilled  water,  and  again  subjected  it 
to  high  muffle  heat.  This  absorbent,  inorganic  cloth  he  applied  to 
buccal  glands  for  twenty  or  thirty  minutes  in  cases  of  erosion,  dis- 
solved the  mucus  obtained  in  distilled  water,  dialyzed  the  salts  out, 
and  examined  the  evaporated  residue  under  the  microscope  and  by 
reagents.  He  found  acid  sodium  phosphate  to  be  the  decalcifying 
agent  in  what  he  called  graphic  (hydroglyphic)  erosions  (Figs.  298 
and  299). 

Head^  found  by  experiment  with  a  1  to  20,000  solution  of  acid 
sodium  phosphate  in  water,  acting  in  the  incubator  at  body  temper- 

1  Dental  Cosmos,  1907. 


EROSION  315 

ature,  that  superficial  decalcification  of  enamel  occurred  after  four- 
teen hours,  and  when  polished  off  it  again  decalcified  in  eight  hours, 
and  was  quite  superficially  decalcified  in  two  days;  that  a  5  per  cent., 
2  per  cent.,  1  per  cent.,  and  1  to  500  solution  acted  under  similar 
conditions  in  seventeen  hours,  and  points  out  that  a  solution  of  1 
to  10,000  and  1  to  20,000  acid  sodium  phosphate  in  alkaline  saliva 
acted  after  eight  and  five  days  only.  He  also  has  shown  that  enamel 
which  was  experimentally  slightly  decalcified,  again  hardened  when 
placed  in  saliva  for  a  time.  He  was,  however,  unable  to  explain  the 
result.^ 

Miller  found  the  slowly  acting  acids  do  not  produce  such  decalci- 
fication as  to  retard  the  abrasive  action  of  brushing  with  a  10  per 
cent,  pumice.  Given,  then,  a  decided  production  of  acid  sodium 
phosphate  by  the  buccal  glands  in  contact  with  the  labial  surfaces 
of  teeth  (Kirk)  for  eight  hours  (the  period  of  sleeping,  and  Head's 
period  of  one  experiment,  see  above),  it  is  quite  reasonable  to  suppose 
that  an  undetermined  percentage  of  acid  sodium  phosphate  dissolved 
in  buccal  mucus,  which  in  total  has  an  acid  reaction  to  litmus  (Tru- 
man, Kirk,  and  others),  is  competent  to  produce  a  superficial  decal- 
cification, which  the  morning  brushing  will  remove.  This  repeated 
for  months  or  years  may  produce  the  effect  seen.  Brubaker,  in  1894, 
immersed  a  tooth  for  a  week  in  a  solution  of  acid  sodium  phosphate, 
subjecting  it  daily  to  tooth-brush  friction,  and  at  the  end  of  that 
time  spots  and  grooves  resembling  erosion  made  their  appearance. 

According  to  Head  and  Kirk,  the  acid  phosphate  does  not  attack 
the  enamel  so  as  to  roughen  it,  but  leaves  it  translucently  smooth  and 
white,  and  this  mildness  of  the  action  of  the  acid  sodium  phosphate 
is  just  the  action  that  would  make  smooth  erosion  with  a  minimum 
of  abrasion.     (See  Miller's  experiments,  p.  306.) 

Head  points  out  "that  1  to  500  lactic  acid  in  water  will  decalcify 
enamel  in  thirty  minutes,  while  the  same  percentage  in  saliva  does 
not  do  so  in  fifteen  days,  but  that  the  inhibitory  effect  of  saliva  is 
overcome  when  the  lactic  acid  has  a  strength  of  1  per  cent."  The 
inhibitory  effect,  therefore,  seems  to  lie  in  the  relative  relations  of 
the  acid  and  alkaline  element,  though  Head  has  shown  that  a  mix- 
ture of  1  per  cent,  solution  of  acid  sodium  phosphate  with  a  1  per 
cent,  solution  of  tribasic  sodium  phosphate,  which  is  capable  of 
turning  blue  litmus  red,  but  not  of  turning  red  litmus  blue,  placed 
the  acid  under  control  so  that  the  mixed  solution  did  not  corrode 
the  tooth  placed  in  it,  which  a  1  per  cent,  solution  of  acid  sodium 
phosphate  in  water  would  do. 

1  Dental  Cosmos,  1910. 


316  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

Regarding  the  production  of  the  abnormal  exudate  from  the  labial 
glands,  Kirk  argues  that  in  diseases  of  suboxidation  (resulting  in 
hyperacid  conditions  such  as  gout  and  rheumatism)  the  blood  is 
loaded  with  carbonic  acid  as  a  result  of  faulty  metabolism.  In  the 
epithelium  of  the  kidneys,  the  mass  action  of  the  carbonic  acid  upon 
the  sodium  phosphate  of  the  blood,  normally  produces  acid  sodium 
phosphate,  which  is  eliminated  in  the  urine,  and  sodium  bicarbonate, 
which  is  returned  to  the  blood  and  maintains  its  alkalinity  (see  p.  96), 
according  to  the  following  reaction:  HNa2P04+H2C03  =  H2NaP04 
+HNaC03.  If  the  amount  of  carbonic  acid  be  of  only  normal  pro- 
duction, this  action  will  result  in  only  a  normal  amount  of  acid 
sodium  phosphate  in  the  urine  and  perspiration;  but  if  in  excess  and 
not  cared  for  by  the  lungs,  skin,  and  kidneys,  the  buccal  glands 
may  also  take  up  the  action  and  excrete  acid  sodium  phosphate 
in  an  identically  similar  manner.  The  acid  calcium  phosphate  is 
also  found  in  the  saliva  at  times,  and  can  be  formed  in  a  similar  way, 
the  calcium  phosphate  being  substituted  for  sodium  phosphate  as 
the  basic  salt. 

Kirk  states  that  in  the  saliva  of  arthritics  there  are  frequently 
found  acid  salts,  such  as  acid  sodium  phosphate  and  acid  calcium 
phosphate.  The  excessive  amount  of  carbonic  acid  accounts  for  the 
excessive  loss  of  phosphate  in  the  kidneys  seen  in  arthritics,  as  the 
acid  sodium  phosphate  and  acid  calcium  phosphate  require  for  their 
production  the  basic  phosphates,  and  the  elimination  of  those,  con- 
tinuously, produces  a  phosphaturia  until  depletion  of  phosphates 
occur,  when  their  amount  lessens  and  other  salts  appear.    (See  p.  96.) 

In  a  paper  published  in  1902,  Kirk^  describes  polariscopic  obser- 
vations made  upon  saliva  from  a  patient  afflicted  with  a  general 
erosive  wasting  of  the  teeth.  The  patient  had  had  attacks  of  in- 
flammatory rheumatism,  and  suffered  from  obstinate  constipation, 
periodic  attacks  of  migraine,  headaches,  and  neuralgia,  and  his 
saliva  was  most  acid  at  night.  The  saliva  was  dialyzed,  the  dialysate 
concentrated,  and  found  to  contain  lactic  acid  salts,  calcium  lacto- 
phosphate,  calcium  lactate,  and  magnesium  lactophosphate  (Fig. 
301). 

In  view  of  these  two  classes  of  cases.  Kirk  has  suggested  that 
erosion  cases  may  be  of  two  kinds:  (1)  A  general  erosion,  in  which 
all  of  the  surfaces  are  uniformly  involved,  and  in  which  lactic  acid  is 
the  solvent  agent;  and  (2)  cases  distinctly  due  to  an  exudate  from 
abnormal  buccal  glands  or  gland,  the  acidity  of  which  is  due  to  either 
acid  sodium  phosphate  or  acid  calcium  phosphate.     Talbot^  claims 

1  Items  of  Interest.  "  Dental  Cosmos,  December,  1907. 


EROSION 


317 


that  the  systemic  acidosis  produced  by  various  diseases  and  by  fruit 
eating  in  excess  is  responsible  for  the  acidity  of  the  buccal  mucus 
and  saliva,  and  for  pulp  and  gingival  degeneration  and  resorption 
through  a  process  of  artery  and  nerve-end  degeneration.  A  decrease 
in  the  normal  acidity  of  the  urine  (below  30)  indicates  renal  insuffi- 
ciency, and  the  difference  indicates  the  amount  retained  in  the 
system.  An  excessive  acidity  of  the  urine  indicates  excessively 
imperfect  oxidation.  This  expression  of  the  cause  is  quite  compatible 
with  the  view  of  Kirk,  and  both  are  views  of  general  malnutrition. 
(See  p.  93,  etc.) 

Fig.  301 


>-Ji 

ip^ 

'^X\ 

t^^l^^  -s 

ife 

L 

^-'" 

k 

J 

^^^K'''^'^' 

^h^'^&9L 

€'•'■■'' 

Crystallization  of  salts  from  dialysate  of  saliva  from  erosion  case,  showing  two  typical 
forms.    Large  crystal  is  calcium  lactate.     (Kirk.) 

The  disease  appears  to  affect  females  more  than  males;  appears 
usually  after  thirty  years  of  age,  and  often  some  history  of  goutiness, 
arthritis,  or  rheumatism  can  be  obtained.  Miller  denied  the  presence 
of  this  disease  in  the  gouty,  but  since  his  observation  the  editor 
has  had  several  patients  hold  up  gouty  fingers  when  questioned  as 
to  a  possible  gout  as  a  cause  of  the  erosions  present. 

Erosion  Due  to  Extraneous  Acids.— Miller^  describes  a  case  re- 
ported by  Davenport,^  of  Paris,  of  a  healthy  man  whose  teeth  were 
eroded  and  worn  away  by  acid  vapors,  within  six  months  of  entering 
a  factory  devoted  to  the  manufacture  of  nitric  and  sulphuric  acids. 
This  effect  was  observed  upon  the  other  workmen  also,  and  also  in 
workmen  in  a  dynamite  factory  in  which  these  acids  are  used.  The 
teeth  were  first  set  on  edge.    Miller  suspended  a  tooth  in  a  flask  con- 


1  Dental  Cosmos,  1907. 


2  Transactions  American  Dental  Association,  1881. 


318  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

taining  equal  parts  of  nitric  and  sulphuric  acid,  and  found  that  the 
vapors  attacked  not  only  the  inorganic  but  the  organic  portion  as 

Fig.  302 


^"'^  tI^^^^I 

i  '-^'' dH 

^^1 

^^^" 

flkv  'J^^l^^^^l 

Another  field  from  the  same  specimen  as  Fig.  301,  also  showing  two  typal  forms. 
Large  crystal  is  calcium  lactate.     (Kirk.) 

Fig.  303 


Crystallization  from  solution  of  a  tooth  in  1  per  cent,  lactic  acid.     Large  crystal  is 
calcium  lactate.     (Kirk.) 

well,  so  that  upon  shght  rubbing  with  a  soft  tooth-brush  the  tissue 
was  worn  away,  leaving  a  hard,  polished  surface.    Miller  states  that 


EROSION  319 

the  vapor  is  nitrogen  peroxid,  N2O4.  Lemon  juice,  even  in  lemonade, 
and  vinegar  will  produce  this  effect  of  setting  on  edge,  which  undoubt- 
edly is  due  to  the  chemical  solution  of  a  small  portion  of  the  enamel, 
probably  the  interprismatic  cement  substance,  leaving  the  enamel 
globules  a  trifle  higher,  this  soon  being  worn  off  to  a  general  level 
again. 

Guilford^  mentions  a  case  of  erosion  caused  by  shaddock  (grape 
fruit)  eating.  Tomes  cites  cases  of  erosion  caused  by  lemon  and 
grape  sucking.  The  pitting  of  grapes  has  produced  cases  of  peculiar 
erosion  of  the  labial  and  lingual  surfaces  and  incisal  edges  of  anterior 
teeth.  In  one  case,  the  incisal  anchorage  of  an  approximal  gold 
filling  was  almost  worn  away  upon  the  tooth  most  used  to  pit  the 
grape.  Unquestionably,  other  fruit  juices  might  act  in  a  similar 
manner  if  the  acid  has  an  affinity  for  tooth  structure,  and  the  expo- 
sure to  its  action  is  sufficiently  lengthy  and  often  enough  repeated 
to  produce  effects. 

The  Effects  of  Erosion. — Tubular  calcification  and  secondary  dentin 
are  produced  together  with  atrophic  changes  in  the  pulp,  due  to 
secondary  dentin  formation.  Gold  and  amalgam  fillings  are  left  as 
raised  islands  by  the  wasting  of  the  tooth  around  them,  though 
Miller  has  shown  that  associated  abrasions  may  cause  their  wear, 
which  acids  evidently  can  hardly  be  expected  to  do. 

Scratches  shown  as  lines  and  Baume's  clefts  are  explainable  upon 
the  theory  of  abrasion  by  brush  and  powders;  though  usually  trans- 
verse, there  are  sometimes  vertical  lines.  The  stimulation  of  the 
dentinal  fibrillse  by  acid  or  mechanical  stimuli  may  cause  great  hyper- 
sensitivity; as  a  rule,  however,  this  is  not  pronounced  (Fig.  304). 

The  anterior  teeth  are  sometimes  shortened  so  that  their  occlusion 
is  lost.  Kirk's  lactic  acid  case  was  of  this  order.  The  carious  process 
may  become  implanted  upon  an  eroded  area,  or  at  some  part  of  it, 
usually  the  cervical  portion.  Whether  this  is  initiated  by  a  decal- 
cifying process  due  to  the  acid  sodium  phosphate,  or  uncleanliness 
due  to  a  cessation  in  the  intensity  of  the  brushing,  is  not  so  clear  as 
it  formerl}^  seemed,  when  it  was  thought  due  to  a  temporary  cessation 
in  production  of  acid  sodium  phosphate,  which  was  regarded  as 
immunizing  the  part  to  caries.  In  any  event  the  stain  of  iodin  is 
taken,  showing  the  presence  of  bacterial  films  at  the  point  showing 
caries. 

Diagnosis. — The  presence  of  the  peculiar  excavations,  the  hyper- 
sensitivity of  dentin  if  any,  and  the  acid  character  of  the  mucus 
from  the  follicles,  as  shown  upon  test  with  litmus  paper  made  just 

1  Lectures. 


320 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 


after  rising/  are  diagnostic  signs.     Kirk's  method  of  obtaining  the 
acid  may  be  used.     (See  p.  314.)    The  acid  reaction  is  not  marked 


PC 


SD 


Fig.  304 


-EC 


Sagittal  action  of  human  incisor  prepared  by  Hopewell-Smith's  process,  and  stamed 
with  hematoxylin:  E  C,  erosion  cavity,  on  surface  of  which  can  be  seen  Baume  s 
clefts;  P,  pulp  tissue  undergoing  degenerative  changes;  F  C,  atrophic  odontoblasts: 
S  D,  secondary  dentin.      X  45.     (Hopewell-Smith.) 


1  Truman. 


EROSION  321 

during  the  day.  The  existence  of  erosion  has  become  a  valuable 
diagnostic  sign  for  the  general  practitioner  in  his  search  for  the 
nature  of  masked  maladies  from  which  patients  frequently  suffer. 

Obscure  gout  has  been  pointed  out  through  dental  indications  alone, 
where  the  practitioner  had  before  been  baffled  in  his  diagnosis. 

Treatment. — The  treatment  of  erosion  divides  itself  under  two 
heads:  Prophylactic  and  restorative;  the  prophylactic  is  again 
divided  into  local  and  general  treatment.  The  problem  of  eradicating 
the  cause  of  the  disorder  lies  in  a  correction  of  the  morbid  glandular 
secretion.  It  is  evident  that  if  the  irritation  and  altered  secretion  of 
these  glands  be  due  to  some  systemic  cause,  a  disease  of  suboxidation, 
notably  an  affection  of  the  gout  order,  a  cure  of  the  local  disturbance 
involves  the  cure  of  the  underlying  systemic  cause.  Talbot^  reduces 
the  acidity  to  normal  with  sodium  bicarbonate  (10  to  30  grains),  or 
sodium  chlorid  (45  grains),  after  meals;  or  sodium  phosphate  morning 
and  evening.  One-tenth  grain  of  calomel  is  given  each  two  hours,  for 
a  time,  to  cleanse  the  bowel  and  stimulate  the  liver.  Eight  to  ten 
glasses  of  water  should  be  taken  daily.  A  practically  antigout  diet 
and  hygiene  are  suggested,  to  increase  oxidation  and  elimination. 
Local  treatment  of  the  gums  is  necessary.     (See  pages  97-105.) 

Kirk,2  working  to  the  end  of  reducing  acid  buccal  secretion,  uses, 
three  times  a  day,  ^li)  grain  pure  phosphorus  in  olive  oil,  in  gelatin 
capsules,  along  with  a  very  mild  laxative,  and  when  the  urine  shows 
a  deficiency  of  phosphates,  25  to  30  grains  per  diem  of  glycerophos- 
phate of  lime  and  soda  are  given. 

Next  in  importance  to  the  prevention  of  acid  formation  is  its 
neutralization.  This  implies  the  application  of  alkalies  or  the  use 
of  alkaline  mouth  washes.  The  greatest  production  of  acid  occurring 
during  the  night,  applications  of  adhesive  masses  of  alkaline  sub- 
stances are  made  to  the  teeth  at  night.  The  principal  of  these  is 
prepared  chalk,  calcium  carbonate;  it  is  rubbed  over  the  labial  faces 
of  the  teeth  and  between  them,  before  retiring.  It  remains  in 
sufficient  amount  to  neutralize  any  acid  substances  coming  in  contact 
with  it. 

Excellent  results,  as  to  the  checking  of  the  progress  of  the  decal- 
cification, are  obtained  from  the  use  of  magnesium  hydrate  held  in 
suspension  in  water,  or  milk  of  magnesia.  Kirk  found  that  three 
hours  after  the  use  of  a  teaspoonful  of  the  milk  of  magnesia,  the 
saliva  maintained  an  alkaline  reaction.  It  should  be  used  at  night 
as  a  wash,  after  cleansing  the  teeth,  the  residue  to  be  left  as  an 
alkaline  coating  upon  the  teeth.     The  chalk  and  milk  of  magnesia 

1  Dental  Cosmos,  December,  1907.  ^  Dental  Cosmos,  190S,  p.  811. 

21 


322  AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 

may  be  mixed  into  a  paste.  If  the  preparation  be  disagreeable,  a 
few  drops  of  essential  oil  may  be  added.  (See  Caries.)  The  abrasive 
factor  and  its  possibilities  as  causes  of  apparent  erosions  suggest  the 
avoidance  of  any  strongly  abrasive  powders,  or,  perhaps,  a  confine- 
ment to  the  use  of  castile  soap  and  a  soft  brush. 

It  has  been  suggested  by  Ottolengui^  that  in  the  earlier  stages  an 
impression  and  plaster  model  of  the  teeth  be  made  for  comparison 
at  future  dates,  so  that  the  progress  of  the  erosion  may  be  noted. 

Restoeative  Treatment. — If  the  eroded  areas  be  excavated  and 
filled,  the  erosion  may  proceed  about  the  edges  of  the  fillings.  It 
may,  however,  take  some  time  for  the  erosion  to  become  as  deep  as 
the  original  area. 

If  metal  be  used,  the  margins  must  be  extended  to  avoid  this,  if 
possible.  Metal  is  very  unsightly  in  the  locations  peculiar  to  erosion, 
so  that  porcelain  inlays,  which  the  locations  favor,  are  indicated.  In 
their  place  silicate  cement  fillings  may  be  used,  but  must  be  constantly 
kept  in  a  good  condition  of  surface  or  they  become  unsightly. 

The  generally  distributed  erosions  are  only  amenable  to  the  prophy- 
lactic treatment  (except  by  crowning,  when  teeth  are  largely  wasted 
away),  and  slight  erosions  are  best  treated  in  the  same  manner.  If 
a  sharp  edge  be  produced  it  is  well  to  remove  it,  as  lip  irritation  may 
possibly  be  a  factor  in  the  acid  production. 

MECHANICAL   INJURY   OF   THE    TEETH. 

The  enamel  is  a  material  much  more  brittle  and  inelastic  than  the 
dentin,  and,  therefore,  less  capable  of  resisting  a  parting  strain. 
Under  ordinary  circumstances,  however,  well-formed  enamel  dis- 
tributed over  sound  dentin  resists  all  the  ordinary  forces  brought 
to  bear  upon  it. 

Under  abnormal  conditions,  however,  enamel  appears  to  fracture 
readily  in  two  directions:  (1)  Along  the  line  of  the  interprismatic 
cement  substance  between  the  prisms  themselves,  and  (2)  along  the 
line  of  cement  substance  between  the  globules.  The  possibility  of 
reference  of  all  cases  into  one  or  other  class  indicates  that  the  cement 
substance  is  naturally  a  tissue  relatively  weak. 

Dentin  may  apparently  fracture  in  any  plane. 

Causes. — The  teeth  may  be  mechanically  injured  by  (1)  the  action 
of  abrasion,  which  mechanically  wears  away  the  teeth;  (2)  by  the 
application  of  undue  force  during  mastication  or  by  the  improper 
use  of  cutting,  filling,  or  extracting  implements;   (3)  by  blows  of 

1  Methods  of  Filling  Teeth. 


MECHANICAL  INJURY  OF  THE  TEETH  323 

some  sort,  delivered  either  directly  upon  the  teeth  or  through  forcible 
closure  of  the  jaws,  as  the  result  of  a  shock  or  blow  delivered  upon 
the  rim  of  the  jaw. 

Aside  from  blows  or  bites  of  sufficient  force  to  break  sound  teeth, 
it  is  rare  to  find  teeth  fractured  without  a  previously  acquired 
weakness  in  the  tooth  itself.     The  causes  of  weakness  are  several. 

During  the  course  of  abrasion  the  enamel  is  worn  to  a  sharp  edge, 
which  is  readily  fractured.  Oblique  splintering  occurs  in  the  line  of 
cement  substance  between  the  globules.  The  enamel  edges  become 
ragged  and  further  fracture  is  imminent.  Thread  biting  produces  a 
similar  but  localized  condition  (Fig.  308). 

Caries,  by  removing  the  natural  support  of  the  enamel,  renders  this 
brittle  material  subject  to  fracture  in  ordinary  use.  The  removal  of 
dentin  from  both  the  mesial  and  distal  sides  of  a  crown  by  caries 
— e.  g.,  a  bicuspid — renders  the  buccal  or  lingual  section  liable  to 
fracture,  as  the  result  of  a  strain  delivered  between  the  cusps  and 
tending  to  wedge  them  apart.  This  accident  is  liable  to  occur  in 
proportion  to  the  lessening  of  the  healthy  dentin  between  the  cavities 
or  beneath  the  occlusal  fissure.  An  upper  incisor  so  decayed  would 
naturally  have  its  labial  section  fractured  away,  particularly  its 
incisal  half. 

The  exposure  of  the  dentin  of  a  devitalized  tooth  to  the  saliva 
seems  to  weaken  it. 

While  these  principles  are  correct,  it  is  surprising  to  what  extent 
enamel  undermined  by  caries  may  retain  its  integrity  if  properly 
supported  by  an  adhesive  oxyphosphate  of  zinc. 

The  packing  of  cohesive  gold  against  frail  enamel  walls  renders 
them  liable  to  direct  fracture,  or  if  packed  so  as  to  permit  leakage 
the  wall  is  further  weakened  by  lactic  acid  produced  upon  its  under 
surface.  Again,  the  improperly  prepared  cavity  margin  may  be 
comminuted,  a  condition  favoring  the  recurrence  of  caries. 

Gold  does  not  support  enamel  walls  so  well  as  oxyphosphate.  If 
built  over  comparatively  frail  walls  in  such  a  manner  as  to  protect 
them  from  direct  impact,  they  stand  fairly  well.  Inlays  of  gold 
serve  a  useful  purpose  in  this  connection.    . 

Amalgam  by  its  attendant  leakage  permits  gradual  weakening  of 
frail  enamel  walls.  The  use  of  a  cement  lining,  as  in  combination 
fillings,  is  distinctly  useful  both  as  a  support  and  prevention  of 
leakage. 

Johnson^  explains  fracture  after  filling,  where  the  enamel  walls 
were  previously  undermined  but  not  fractured,  upon  the  theory  that 

.  1  Principles  and  Practice  of  Filling  Teeth. 


324 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 


Fig.  305 


previous  to  filling,  the  pain  attendant  upon  mastication  brings  about 
a  temporary  disuse  of  the  diseased  tooth.  After  filling,  comfort 
ensues,  the  patient  again  uses  the  tooth,  and  fracture  occurs. 

The  fractures  caused  by  blows  present  features  of  interest.  An 
actual  splitting  off  of  one  of  the  angular  portions  of  a  crown  may 
occur,  or  a  fracture  may  be  seen  resembling  one  sometimes  seen  in 
a  pane  of  glass,  the  result  of  a  light  blow  from  a  stone. 

In  the  latter  case,  the  cracks  radiate  from  a  central  crushed  spot, 
and  may  involve  only  the  enamel.  A  large  section  of  an  incisor  may 
be  fractured  away  and  include  the  labio-incisal  third  and  all  the 
lingual  section  of  the  crown  and  a  small,  ob- 
liquely fractured  portion  of  the  root.  This 
results  from  a  blow — %he  exact  opposite 
usually  results  from  occlusal  strain. 

Biting  upon  hard  objects  has  caused  the 
fracture  of  sound  bicuspids  and  molars,  the 
line  extending  mesodistally  between  the 
cusps,  the  fracture  being  oblique  or  through 
the  crown  and  between  the  roots.  Thus  a 
molar  or  first  bicuspid  may  be  divided  into 
two  sections,  each  supported  by  a  root  or 
roots  (Figs.  306  and  307). 

Fracture  and  repair  of  enamel  after  erup- 
tion is  not,  so  far  as  I  am  aware,  known. 
Cases  of  fracture  and  repair  of  dentin  have 
occurred. 

A  case  of  such  repair  by  adventitious  (sec- 
ondary) dentin  has  been  recorded  by  Tomes,^ 
and  Fig.  309  illustrates  a  fracture  of  the 
root  well  below  the  gum  line.  The  root  is 
girdled  by  the  line  of  fracture,  but  the  dentin 
has  been  repaired,  and  the  attachment  is 
firm.  The  line  evidently  indicates  a  repair 
from  the  pulp  side.  A  case  analogous  to  heal- 
ing of  a  comminuted  fracture  of  a  central  has 
been  reported. ^  Fig.  310  illustrates  a  peculiar  fracture  due  to  an 
unknown  cause.     (See  p.  326.) 

In  a  case  reported  by  Val.  Macdonald,^  of  a  similar  fracture,  the 
pulp  maintained  its  vitality  in  both  crown  and  root  for  two  years, 
and  until  the  tooth  was  extracted.  There  was  between  crown  and 
root,  a  growth  of  soft  tissue  connected  with  both  the  pulp  and  the 

1  A  System  of  Dental  Surgery.     (See  Secondary  Dentin.) 

2  Watson:  Dental  Record,  May,  1906.  ^  Dental  Cosmos,  January,  1908. 


Fracture  of  two  years' 
standing  with  pulp  vital 
and  a  lateral  tissue  growth 
resembling  granulation  tis- 
sue covering  the  root  face, 
would  explain  how  the 
case.  Fig.  309,  occurred. 
(Macdonald.) 


MECHANICAL  INJURY  OF  THE  TEETH 


325 


pericementum,  and  considered  by  Macdonald  to  be  pulpal  in  origin 
(Fig.  305).    Macdonald's  case  would  explain  that  in  Fig.  309. 

In  an  experimental  implantation  of  a  dried  tooth,  filed  to  fit  the 
socket  of  a  previously  extracted  tooth,  union  of  osseous  nature  took 
place,  and  a  slight  fracture  of  the  root  was  reunited  by  osseous 
deposition.^ 


Fig.  306 


Fig.  307 


Oblique  fracture. 


Fracture  involving  the  bifurcation  of  the  roots. 


Longitudinal  cracks  in  the  enamel  of  otherwise  fairly  sound  teeth 
occur,  the  line  running  from  the  labial  edge  of  the  gum  to  the  incisal 
edge  of  an  incisor  (Fig.  308),  or  from  the  fissure  of  a  bicuspid  along 
the  enamel  to  the  summit  of  a  cusp,  or  from  the  cervical  margin  of 
an  approximal  cavity  to  the  gum  margin. 


Fig.  308 


Fig    309 


Abrasion  associated  with  fracture  of  the 
enamel. 


Root  fracture  and  reattachment  by  ad- 
ventitious dentin.   (From  a  specimen.) 


These  lines  probably  indicate  that  force  has  been  applied,  sufficient 
to  cause  a  parting  of  the  enamel  cap  without  loss  of  continuity  in 
the  more  elastic  dentin.  Dryness  from  mouth  breathing  may  be  a 
possible  cause  of  cracks,  and  the  contact  of  excessively  hot  or  cold 


'  Mendel  Joseph  and  Dessonville:  L'Odontologie.    (See  Cosmos,  1904,  p.  1060.) 


326 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 


substances  has  been  advanced  as  an  hypothesis,  but  mostly  they  are 
found  in  cases  of  overworked  teeth.  In  some  cases  the  enamel 
cracks  may  be  very  numerous.  These  cracks  take  up  stains,  and  at 
times  in  the  preparation  of  cavities,  cause  annoyance  by  centring 
the  chisel  and  perpetuating  a  defect,  necessitating  the  removal  of 
much  tooth  tissue  or  the  risking  of  future  caries.  In  one  case  typical 
of  a  class  of  accidents,  the  root  of  a  second  bicuspid  was  found  loose 
and  fractured  longitudinally  (Fig.  310).  As  its  occlusal  end  was 
firmly  embedded  in  an  encircling  crown  band,  and  no  pins  had  been 
used,  the  only  explanation  seems  to  be,  fracture  in  preparation,  the 
swelling  of  the  guttapercha  root  canal  filling  or  the  expansion  of  gas. 
Such  an  explanation  could  not  apply  to  the  fracture  in  Fig.  311. 

Fig.  310 


Case  of  root  fracture.     (See  Text.) 


Treatment. — The  treatment  of  fractures  involves  considerations 
purely  operative,  and  depends  upon  the  nature  of  the  case.  Rough- 
ened, abraded  enamel  margins  are  best  rounded  with  carborundum 
stones  or  coarse  sand-paper  disks,  and  should  be  polished.  Some- 
times a  deep  serration  must  be  filled;  corners  are  to  be  nearly  rounded 
or  restored  to  contour  by  fillings  or  inlays,  or  at  times  the  entire 
incisal  edge  is  to  be  ground  away  and  the  tooth  drawn  down  and 
retained  until  firm. 

In  case  of  an  uncompleted  tooth  root,  and  the  pulp  not  quite 
exposed,  a  pure  gold,  all-metal  crown  is  to  be  adapted  with  or  without 
grinding,  according  to  the  future  requirements,  and  the  root  com- 
pletion awaited.  If  necessary,  the  capping  of  the  pulp  may  be 
attempted  as  well,  for  the  same  purpose. 

After  root  formation  the  pulp  may  be  destroyed  if  desired.  If 
conservation  of  the  pulp  be  not  possible,  the  pulp  may  be  prepared 
for  removal  by  pressure  anesthesia  or  conductive  anesthesia,  and  the 
root  filled.     (See  Root  Fillings.) 

Fractures  involving  the  cementum  demand  either  the  removal  of 


MECHANICAL  INJURY  OF  THE  TEETH 


327 


the  loosened  piece  and  the  construction  of  a  special  crown  retaining 
a  portion  of  the  natural  crown  as  a  base,  or  the  removal  of  all  of  the 
natural  crown  and  the  mounting  of  a  substitute  upon  the  root,  or  the 
parts  may  be  banded,  or  in  case  of  molars  an  all-metal  crown  may 
be  mounted.  In  some  cases  screws  or  a  staple  must  be  placed  in  the 
roots  and  the  parts  restored  with  amalgam  (Figs.  313  to  315).  If 
the  loosened  portion  be  retained,  thin  oxychlorid  of  zinc  is  to  be 
introduced  into  the  joint  after  appropriate  sterilization,  and  before 
the  gold  crown  or  holding  device  is  set.  It  distributes  itself  by  capil- 
larity, if  the  joint  is  slightly  opened  once  or  twice.  The  split  piece, 
if  of  the  oblique  type,  is  apt  to  irritate,  and  in  most  cases  in  time 
cause  lateral  abscess.  It  should  ordinarily  be  removed  and  the  part 
prepared  as  in  Fig.  313.     Should  the  pulp  be  vital  at  the  time  of 


Fig.  311 


Fig. 312 


Fracture  of  portion  of  upper  cuspid, 
cause  unknown.  (Skiagraph  by  E.  Ball- 
ard Lodge.) 


Fracture  with  dovetails  for  amalgam. 
(Evans.) 

Fig.  313 


Oblique  fracture  of  root,  with  pin  and 
amalgam  for  restoration,  ready  for 
crowning.      (Evans.) 


fracture,  it  will  become  inflamed,  and  should  be  removed  by  the 
pressure  method  if  possible.  To  accomplish  this,  the  parts  must 
be  lashed  together  and  an  occlusal  opening  made.  After  devitali- 
zation, the  parts  may  be  given  a  dove-tailed  form,  and  be  temporarily 
held  together,  internally,  by  amalgam,  or  a  circular  band  may  be 
inlaid  in  a  trephined  groove  by  Cigrand's  method  (Fig.  3160-  The 
cuspid  root  shown  in  Fig.  314  had  an  amalgam  filling  in  its  mesial 
side  until  after  the  cap  and  band  were  constructed.  A  temporary 
crown  caused  the  wall  to  fracture  out,  so  the  plan  was  devised  of 
drilling  holes  in  the  root  side,  tapping  them  with  the  How  tap  and 


1  For  certain  crowning  devices  in  cases  of  fracture,  see  Evans'  Crown  and  Bridge- 
work,  and  Goslee's  Principles  and  Practice  of  Crowning  Teeth. 


328 


AFFECTIONS  OF  THE  ENAMEL  AND  DENTIN 


placing  iridioplatinum  screws  on  both  sides  of  the  pulp  canal  groove. 
The  pin  and  cap  were  then  waxed  slightly,  placed  in  position,  amal- 
gam built  in  and  when  hard,  the  wax  was  melted  by  heating  the 


Fig.  314 


Fig.  315 


Screws  placed  into  a  fractured  root  to 
enable  the  building  up  of  amalagam 
around  a  waxed  pin  attached  to  a  gold- 
cap.  This  root  is  one  of  four  piers 
of  a  nine-tooth  bridge. 

Fig. 


Staple  used  to  unite  portions  of  a 
fractured  root.     (Evans.) 


316 


?    i 


Cigrand's  method  of  trephining  a  root  face  and  inlaying  a  metal  ring;  also  useful  to 
prevent  fracture  when  plain  dowel  crowns  are  used. 


cap  and  pin,  which  were  withdrawn.  After  thorough  hardening, 
the  bridge- work  was  proceeded  with.  Fortunately  the  root  received 
its  strain  from  the  lingual  side,  which  was  largely  intact.  The 
requirements  vary,  and  must  have  due  consideration. 


CHAPTER  X. 

STAINS  OF  THE  ENAMEL  AND  DENTIN. 

Certain  stains  are  found  upon  the  surface  of  the  enamel  and  some- 
times penetrating  its  substance.  The  calculus  sometimes  located 
upon  the  enamel  is  not  included  in  this  consideration,  though  the 
calculus  itself  sometimes  becomes  stained.  So  far  as  they  have 
been  observed,  stains  may  be  divided  into  those  of  metallic  and 
non-metallic  origin. 

METALLIC   STAINS. 

Metallic  stains  are  those  which  are  caused  by  the  direct  depo- 
sition of  minute  particles  of  metal,  inhaled  by  workers  in  the  metals, 
in  the  organic  collections  upon  the  surfaces  of  the  teeth,  or  taken 
into  the  mouth  in  various  solutions  of  drugs. 

Copper. — Miller  found  that  "workers  in  copper,  brass,  or  bronze 
all  presented  a  green  stain  upon  the  upper  teeth,  showing  every  shade 
of  green  and  bluish-green  up  to  bluish-purple.  The  latter  color  pre- 
dominated in  rooms  where  phosphor-bronze  was  worked."  Attention 
is  called  to  the  fact  that  "trumpeters  very  often  show  a  discolor- 
ation of  the  teeth."  Similar  discolorations  are  sometimes  noted  in 
proximity  to  copper  amalgam  fillings.  The  presence  of  copper  was 
demonstrated  in  scrapings  from  some  of  the  stained  teeth,  imparting 
a  characteristic  green  color  to  a  Bunsen  flame.  McGeehee^  notes 
a  case  of  a  metal  worker  whose  enamel  was  stained  and  the  dentin 
as  well,  the  tooth  being  vital.  The  presence  of  defects  or  spaces 
containing  organic  matter  is  evidenced  (see  p.  352).  Bands  or  wires 
containing  base  metals,  generally  containing  copper,  sometimes  stain 
enamel. 

Iron. — "Workers  in  iron  presented  stains  of  a  brownish  color." 
As  pointed  out,  "the  green  salts  of  iron  under  the  conditions  found 
in  the  mouth  would  become  oxidized  and  brownish  in  color."  The 
administration  of  iron  salts,  medicinally,  is  believed  to  produce 
black  discolorations,  iron  sulphid  being  formed.  "Iron  deposits  are 
usual  in  the  border-line  between  carious  and  normal  dentin."  It  is 
believed  that  the  brownish  spots  frequently  seen  in  connection  with 

1  Dental  Cosmos,  March,  1912. 

(329) 


330  STAINS  OF  THE  ENAMEL  AND  DENTIN 

incipient  or  arrested  caries  of  the  enamel  are  due  to  the  formation 
of  iron  salts.    Iron  or  steel  in  dentin  stains  black  with  iron  sulphid. 

Manganese. — Manganese  was  found  in  the  dark  colored  deposits 
upon  the  teeth  of  herbivorous  animals,  but  as  yet  not  upon  those  of 
man.  The  investigator  stated  "that  alkaline  saliva  may  be  necessary 
to  the  production  of  these  deposits."  Manganese  stains  may  occur 
from  the  use  of  potassium  permanganate,  manganic  oxid  being 
formed. 

Mercury. — In  cases  of  prolonged  mercurial  administration  the 
deposits  (black)  upon  the  teeth  may  give  the  reaction  for  mercury. 
"If  mercury  and  potassium  iodid  are  given  together,  the  green  iodid 
of  mercury  might  be  present  upon  the  teeth."  It  is  probable  in  these 
cases  that  another  discoloring  substance  may  form.  There  is  in 
mercurialism  more  or  less  gingivitis;  the  gums  are  swollen  and 
spongy,  bleeding  readily.  "More  or  less  putrefactive  decomposi- 
tion of  the  albuminous  matter  present  upon  the  teeth  occurs,  and 
hydrogen  sulphid  is  formed.  Reacting  upon  the  oxyhemoglobin  of 
the  blood,  sulphomethmoglobin  is  formed — greenish  red  in  concen- 
trated, green  in  dilute  solutions."  Miller  ascribes  the  discoloration 
found  in  conditions  of  gingivitis  from  various  causes,  with  lack  of 
hygienic  care,  to  a  probable  reaction  between  hydrogen  sulphid  and 
oxyhemoglobin. 

Lead. — Hirt  (quoted  by  Miller)  found  in  cases  of  lead  poisoning, 
discolorations  upon  the  teeth :  dark  brown  at  the  necks,  light  brown 
on  the  crowns,  with  sometimes  a  trace  of  yellowish  green.  Miller's 
tests  (limited  in  number)  showed  no  lead  reaction  from  the  dental 
deposits  in  lead  poisoning. 

Nickel. — Some  of  the  salts  of  nickel  are  green.  Metallic  nickel 
attacked  by  jfluids  of  the  mouth  and  mixtures  of  bread  and  saliva  pro- 
duces greenish  salts.  The  entire  root  of  a  tooth  containing  a  nickel 
retaining  screw  has  been  stained  a  uniform  apple  green. 

Silver. — The  dentin  of  pulpless  teeth  containing  amalgam  fillings 
is  sometimes  stained  black,  owing  to  the  formation  of  silver 
sulphid. 

The  use  of  silver  nitrate  as  a  wash  may  cause  the  albuminate  of 
silver  to  precipitate  salts  of  silver  upon  the  teeth.  If  a  cavity  be 
touched  with  silver  nitrate  and  an  amalgam  filling  be  introduced, 
the  salts  of  silver  will  be  instantly  formed  at  any  point  where  the 
silver  nitrate  and  amalgam  combine.  If  this  be  upon  the  enamel,  the 
latter  will  receive  a  somewhat  lasting  black  stain. 

The  nitrate  of  silver  applied  to  dentin  causes  the  dentin  to  assume 
a  light  yellowish  green  tinge,  and  the  albuminate  of  silver  is  formed ; 
later  metallic  silver  is  precipitated,  the  tissue  becoming  black. 


NON-METALLIC  STAINS  331 

Gold. — Gold  chloric!  stains  may  be  formed  during  the  bleaching 
of  teeth  containing  gold  fillings  by  the  chlorin  methods.  The  dentin 
becomes  first  pink,  then  violet  or  purple,  then  black.^ 

NON-METALLIC    STAINS. 

Green  Stain. — The  most  common  of  green  deposits  upon  enamel 
occurs  upon  both  the  temporary  and  the  permanent  teeth,  particu- 
larly of  young  persons.  The  deposits  usually  have  a  crescentic  form, 
are  mainly  upon  the  labial  faces  of  the  anterior  teeth,  and  may  be 
but  a  narrow  line  or  may  cover  one-half  the  labial  face.  It  is  unusual 
for  the  deposit  to  extend  far  into  the  interproximal  spaces,  their 
tendency  being  to  follow  the  edges  of  the  approximal  surfaces.  While 
green  stain  undoubtedly  does  form  upon  adult  teeth  (Figs.  317  and 
318),  where  clearly  the  enamel  cuticle  has  long  been  absent,  it  is  only 
very  common  upon  young  teeth  where  remnants  of  Nasmyth's  mem- 
brane persist  about  their  necks.  The  color  of  these  deposits  varies 
from  light  green  to  greenish  black. 

Fig.  317 


Extension  of  green  stain  on  the  approx-  Extension  of  green  stain  on  the  lingual 

imal  surface  of  the  incisors.   (Miller.)  surface  of  the  incisors.    (Miller.) 

If  an  instrument  be  passed  over  the  portion  of  enamel  affected, 
more  or  less  roughness  of  the  surface  is  evident.  If  the  deposits  are 
subjected  to  friction  with  abrasives,  they  disappear  slowly  and  the 
enamel  beneath  may  be  found  roughened.  This  has  led  to  the  belief 
that  these  deposits  cause  decalcification  of  the  enamel.  It  is  found 
upon  adult  teeth  that  when  an  area  of  cervicolabial  enamel  has 
become  roughened  through  slight  decalcification,  a  green  stain  is 
likely  to  form  upon  the  rough  surface,  if  proper  hygienic  care  be  not 
exercised.  It  is  also  found  that  if  the  stain  be  removed  by  means  of 
abrasives,  the  roughened  enamel  may  be  readily  polished — i.  e.,  the 
decalcification  is  very  superficial. 

1  Kirk:  American  Text-book  of  Operative  Dentistry. 


332  STAINS  OF  THE  ENAMEL  AND  DENTIN 

If  cases  be  observed  early  enough  in  childhood,  it  will  be  noted  that 
green  stain  is  usually  preceded  by  a  lack  of  oral  hygiene;  collections 
of  food  debris  are  not  removed  from  about  the  necks  of  the  teeth, 
which  implies  that  prior  to  the  formation  of  green  stain  the  affected 
enamel  surfaces  have  been  subjected  to  the  action  of  fermenting 
food  debris — that  is,  to  acids.  These  facts  have  led  to  an  acceptance 
of  the  view  that  the  roughness  or  decalcification  has  preceded  the 
green  deposits.  "If  teeth  be  placed  in  a  10  per  cent,  solution  of 
hydrochloric  acid,  in  from  two  to  four  minutes  the  enamel  cuticle 
begins  to  loosen,  and  in  from  five  to  ten  minutes  is  isolated.  It  is 
found  that  the  entire  stain  comes  away  with  the  cuticle." 

In  even  the  mouths  of  children,  the  removal  of  green  stain  with 
pumice  may  be  difficult,  showing  that  some  penetration  of  enamel 
substance  has  occurred. 

Nature  of  the  Coloring  Matter. — The  coloring  matter  is  found  to 
be  insoluble  in  water,  glycerin,  alcohol,  ether,  chloroform,  or  oil  of 
turpentine.  Mineral  acids,  hydrochloric,  nitric,  and  nitrohydro- 
chloric  act  but  slowly  upon  the  coloring  matter;  even  hydrochloric 
acid  requires  some  hours  to  completely  destroy  it.  Tincture  of 
iodin,  commonly  believed  to  act  as  a  solvent  of  green  stain,  was 
found  to  affect  it  but  slightly.  Both  chlorin  and  nascent  oxygen 
destroy  the  coloring  matter  rapidly,  the  cuticle  being  bleached  in  a 
few  minutes  by  a  10  per  cent,  solution  of  hydrogen  dioxid.  Thick, 
dark  green  deposits  were  incompletely  bleached  after  eight  hours' 
immersion  in  the  10  per  cent.  H2O2  solution,  pointing  to  a  lack  of 
uniformity  in  the  composition  of  the  stain. 

The  belief  that  the  green  coloring  matter  is  chlorophyl  is  contra- 
dicted by  the  fact  that  it  is  not  soluble  in  ether. 

Miller^  regarded  the  association  of  the  green  discoloration  with 
sulphomethemoglobin,  or  some  allied  substance,  as  the  most  probable 
explanation,  though  he  found  a  micrococcus  in  a  deposit  of  green 
stain  which  produced  a  grayish-green  color  in  glycerin  agar. 

Miller  did  not  find  any  definite  connection  between  a  milk  diet 
and  green  stain. 

Goadby^  has  found  Bacillus  liquefaciens  fluorescens  motilis  present 
in  several  cases  of  green  stain.  It  deposits  in  its  culture  medium 
a  fluorescent  blue-green  pigment.  Other  mouth  bacteria  produce  a 
greenish  pigment — e.  g.,  Bacillus  pyocyaneus  and  Bacillus  fluorescens 
non-liquefaciens.^  The  deposits  of  green  stain  are  considered  to  be 
secondary  to  enamel  decalciflcation  rather  than  the  cause  of  it, 
when  found  in  connection  with  it. 

'  Dental  Cosmos,  1894.  2  Mycology  of  the  Mouth. 

3  Ibid. 


NON-METALLIC  STAINS  333 

In  case  of  roughened  enamel,  green  stain  appears  at  times  to  have 
been  taken  into  its  substance,  rendering  removal  without  bleaching 
difficult. 

Black  Stain. — A  peculiar  black  stain  occurs  in  the  mouths  of  appar- 
ently healthy  individuals,  both  men  and  women,  and  smokers  and 
non-smokers,  and  even  with  those  also  who  drink  neither  tea  nor 
coffee.  It  occupies  the  general  position  described  for  green  stain, 
but  may  cover  much  of  the  surface  of  the  teeth.  It  occurs  in  some- 
what unclean  mouths,  though  the  teeth  may  have  been  regularly 
brushed.  As  a  rule,  those  teeth  having  the  deposit  are  comparatively 
free  from  caries.  Its  etiology  is  not  worked  out,  but  it  may  be  due  to 
a  formation  of  iron  sulphid  in  place  of  sulphomethemoglobin.  It  is 
very  readily  removed,  and  does  not,  as  a  rule,  affect  the  enamel.  At 
times  a  superficial  caries  is  found  associated  with  it,  and  at  some 
minute  spot  the  enamel  may  be  penetrated.  Whether  this  cavity 
is  a  result  of  the  action  of  the  film  is  not  certain.  In  a  case  of  a 
woman  a  black  stain  was  prevalent  for  years — recently  it  has  entirely 
disappeared.  The  only  available  explanation  other  than  some 
possible  unknown  systemic  change,  is  the  use  of  a  well-known  tooth 
paste  which  contains  a  large  percentage  of  potassium  chlorate. 

Tobacco  Stains. — Smokers  have  characteristic  black  deposits  upon 
both  the  teeth  and  calculus  deposited  upon  them.  The  stain  is  most 
marked  upon  the  lingual  surfaces  of  the  teeth,  and  a  pipestem  held 
well  back  in  the  mouth  may  cause  a  thick  deposit  upon  some  of 
the  posterior  teeth. 

Tobacco  juice  itself  stains  exposed  dentin  and  cementum,  and 
enters  cracks  in  the  enamel,  producing  brown  discolorations  very 
difficult  or  impossible  to  remove.  McGeehee  found  tobacco  stain 
to  have  deeply  penetrated  the  enamel  tissue. 

Stains  Due  to  Dyes, — McGeehee^  has  shown  that  colored  mouth 
washes  containing  vegetable  or  analine  coloring  matter  may  stain 
enamel  and  other  tooth  structure.     The  chewing  of  betel  nut  or 
other  material  containing  vegetable    coloring  matter  also  produces , 
a  stain  characteristic  of  the  coloring  element.    Dyed  cotton  also  stains. 

Red  Stain. — A  pecuhar  red  stain  occurs  upon  the  necks  of  some 
teeth,  but  is  not  generally  distributed.  It  is  probably  due  to 
chromogenic  bacteria,  as  it  is  only  found  on  unclean  surfaces. 

According  to  Goadby,^  Bacillus  prodigiosus.  Bacillus  rouge  de  Kiel, 
Bacillus  mesentericus  ruber.  Bacillus  roseus,  Sarcina  roseus.  Micro- 
coccus roseus,  and  other  micrococci  produce  a  red  pigment  in  at 
least  some  of  their  media. 

1  Dental  Cosmos,  March  1912.  ^  Mycology  of  the  Mouth. 


334  STAINS  OF  THE  ENAMEL  AND  DENTIN 

Sarcina  lutea  and  Sarcina  aurantiaca  produce  yellow  and  orange- 
colored  pigment  respectively.^  The  exact  relation  of  chromogenic 
bacteria  to  stains  is  not  worked  out. 


DENTIN   STAINS. 

Exposed  dentin  may  be  stained  as  enamel  is.  In  addition  it  may 
take  up  certain  stains  like  tobacco. 

Metallic  fillings,  such  as  amalgam,  containing  mercury,  silver, 
copper  or  cadmium  metals  which  combine  with  sulphuretted  hydro- 
gen to  form  sulphids,  may  cause  staining  of  dentin. 

Metallic  posts  containing  silver,  copper,  or  nickel,  or  made  of 
steel  or  iron  wire,  may  produce  sulphids  in  the  same  manner.  The 
dentin  may  also  be  stained  pink  by  hemoglobin  entering  the  tubules 
during  the  progress  of  venous  hyperemia.  This  finally  develops 
iron  sulphid. 

The  dentin  may  also  be  stained  by  iron  sulphid  formed  during 
putrefaction  of  the  pulp,  by  the  action  of  ammonium  sulphid  upon 
the  iron  contained  in  the  hemoglobin  of  the  blood  undergoing 
decomposition. 

TREATMENT    OF    STAINS. 

Enamel  stains  are  best  removed  by  mechanical  means,  after  the 
removal  of  calculus  from  the  teeth.  (See  Salivary  Calculus.)  For 
this  purpose,  brush  wheels  and  rubber  cups  charged  with  pumice  and 
revolved  in  the  dental  engine  are  used  to  remove  the  accessible  por- 
tions of  the  stains.  Next  a  wood  point,  made  by  sharpening  an 
orange-wood  stick  or  hickory  shoe-peg  to  a  wedge-shape,  is  charged 
with  the  pumice  and  rubbed  by  hand  over  all  the  surfaces  not  reached 
by  the  brushes  and  cups.  For  the  more  inaccessible  situations,  the 
point  is  to  be  mounted  in  a  Jack  or  other  porte  polisher.  A  very  fine 
linen  tape,  a  German  silver  strip,  or  flat  floss  silk  charged  with 
pumice  will  remove  the  stains  at  the  contact  points.  A  very  small 
finishing  bur  or  dull  ordinary  No.  1  or  No.  |  bur  is  useful  upon 
lingual  surfaces  or  in  grooves. 

The  powdered  pumice  used  is  best  mixed  with  glycerin,  to  prevent 
the  flying  of  the  pumice  during  the  rapid  revolution  of  the  wheels. 
Saturation  of  the  stains  with  tincture  of  iodin  followed  by  a  douche 
of  water  renders  them  more  visible,  and  also  brings  to  view  the 
associated  bacterial  films  upon  the  teeth. 

1  Mycology  of  the  Mouth. 


TREATMENT  OF   STAINS  335 

Register  recommends  the  use  of  1  per  cent,  hydrogen  dioxid,  to 
be  forcibly  sprayed  upon  the  gums  and  deposits  both  before  and 
after  the  use  of  tincture  of  iodin.  The  brush  and  pumice  will  then 
rapidly  remove  the  stains  and  bacterial  films  upon  the  accessible 
portions  of  the  teeth. 

Tobacco  stains  in  cementum  need  not  be  removed  to  their  full  depth. 

Head"^  has  suggested  the  removal  of  deep  enamel  stains  and  the 
deposits  in  irregular  depressions  and  joints  of  inlays,  inaccessible  to 
the  stick,  by  the  use  of  nascent  oxygen  derived  from  25  per  cent, 
ethereal  pyrozone,  or  a  paste  of  sodium  dioxid  and  water,  made  by 
dissolving  the  latter  in  distilled  water  at  about  32°  F.  These  are 
applied  to  the  part  on  cotton,  and  nascent  oxygen  liberated  with  a 
hot  burnisher.  The  face  and  gums  are  protected  by  the  securely 
placed  rubber  dam  and  by  oiling  the  face. 

The  method  is  also  applicable  to  the  bleaching  of  obstinate  stains 
of  the  dentin,  especially  near  the  cutting  edges. 

In  the  joints  of  inlays,  fresh  cement  is  to  be  rubbed — preferably 
the  silicates — in  order  to  prevent  a  rediscoloration. 

If  beneath  green  stains  decalcification  be  discovered,  the  decal- 
cified area  should  be  polished  as  well  as  possible,  but  not  cut  away 
unless  carious  and  the  patient  urged  to  careful  prophylaxis. 

After  the  removal  of  calculus  and  stains  from  the  teeth,  the  mouth 
and  teeth  should  be  kept  in  as  cleanly  and  aseptic  a  state  as  possible, 
by  the  employment  of  correct  prophylactic  measures.  Dental  caries 
and  pyorrhea  alveolaris  are  thus  also  largely  prevented.  (See  Pro- 
phylaxis of  Dental  Caries  and  Pyorrhea  Alveolaris.) 

The  stains  found  in  the  dentin  are  also  divisible  into  metallic  and 
non-metallic.  The  former  are  best  removed  by  transforming  the 
insoluble  metallic  salt  into  a  soluble  one. 

The  most  frequent  and  practicable  course  is  to  form  soluble  chlorids 
through  the  action  of  nascent  chlorin.  Copper,  nickel,  gold,  and 
iron  stains  should  be  subjected  to  the  chlorin  method  of  bleaching, 
followed  by  repeated  washings  with  chlorin  water,  50  per  cent.,  and 
hot  distilled  water  to  remove  the  chlorid  formed.^ 

Silver  stains  are  converted  into  silver  chlorid  by  the  chlorin 
method,  or  iodid  by  the  use  of  tincture  of  iodin,  and  dissolved  out  by 
the  use  of  sodium  hyposulphite,  followed  by  hot  distilled  water.^ 

For  mercurial  stains  Kirk  recommends  the  use  of  aqueous,  ammo- 
niacal  solution  of  hydrogen  dioxid  after  the  chlorin  method,  and  a 
saturated  solution  of  potassium  iodid  after  the  iodin  method,  in 
either  case  followed  by  washing  with  hot  distilled  water. 

1  Items  of  Interest,  1902.  2  Kirk.  3  Ibid. 


336  STAINS  OF  THE  ENAMEL  AND  DENTIN 

Manganese  stain  is  removable  by  the  use  of  25  per  cent,  aqueous 
solution  of  hydrogen  dioxid,  saturated  with  oxalic  acid  crystals  and 
followed  by  washing  with  hot  water. 

The  non-metallic  dentin  stains  are  removable  by  the  use  of  chlorin 
evolved  from  chlorinated  lime  by  the  reaction  with  dilute  acetic 
acid,  or  of  nascent  oxygen  evolved  from  hydrogen  dioxid  or  sodium 
dioxid. 

In  either  case  the  color  molecule  is  destroyed  by  the  indirect  or 
direct  oxidizing  effect. 

The  hydrogen  dioxid  may  be  used  in  the  form  of  the  25  per  cent, 
ethereal  solution  (25  per  cent,  pyrozone)  applied  for  a  time,  or  sealed 
within  the  tooth  for  twenty-four  hours,  or  the  25  per  cent,  aqueous 
solution  may  be  driven  into  the  tubuli  by  the  aid  of  the  cataphoric 
current. 

Sodium  dioxid  should  be  employed  in  saturated  solution  in  distilled 
water  (made  at  about  32°  F.).  The  dentin  is  first  desiccated  and 
then  saturated  with  the  solution.  Weak  sulphuric  acid  (10  per 
cent.)  is  used  to  liberate  the  nascent  oxygen.  Kirk  recommends  a 
second  application,  omitting  the  use  of  the  acid. 

As  with  metallic  stains,  all  the  by-products  should  be  washed  out 
with  hot  distilled  water.  ^ 

A  further  description  will  be  given  under  the  caption  of  Moist 
Gangrene  of  the  Pulp. 

1  For  a  complete  description  of  the  bleaching  process,  see  Kirk's  article  in  American 
Text-book  of  Operative  Dentistry. 


CHAPTER  XI. 

DENTAL  CARIES:  HISTORY;  EXCITING  AND  PRE- 
DISPOSING CAUSES. 

Definition.— Dental  caries  may  be  defined  as  a  disease  of  a  tooth 
characterized  chiefly  by  the  production  of  a  localized  cavity,  con- 
cavity, or  area  containing  decalcified  tooth  structure  and  due  to  a 
combined  acid  fermentation  and  liquefaction. 

History.— Examinations  of  crania  show  the  disease  to  be  certainly 
as  old  as  semicivilization,  and  when  more  data  are  obtainable  it 
will,  no  doubt,  be  found  even  older.  The  skull  of  a  mummy  in  the 
British  Museum,  dating  2800  B.C.,  exhibits  well-marked  caries  and 
other  dental  diseases.  Caries  appears  in  the  teeth  of  the  skulls  of 
all  peoples,  no  matter  what  their  degree  of  civilization,  provided 
their  dietary  included  cooked,  starchy  foods. 

Causes.— These  may  be  divided  into  exciting  and  predisposing. 

Prior  to  the  investigations  of  Miller,^  published  in  1882,  a  vast 
amount  of  labor  was  expended  in  the  effort  to  determine  the  cause 
of  dental  caries.  The  deductions  made  were  partly  speculative  and 
partly  based  upon  scientific  investigations. 

From  1754  to  1835  caries  was  regarded  as  an  inflammation  or 
gangrene  of  tooth  structure;  Boudett,  Jourdain,  Hunter,  Fox,  Bell, 
Fitch,  and  Koecker  advancing  one  or  the  other  theory.^ 

In  1835  Robertson,^  of  Birmingham,  England,  advanced  the 
opinion,  based  upon  his  observations,  that  it  "  is  to  chemical  and  not 
to  inflammatory  action  that  the  destruction  of  the  teeth  must  be 
attributed."  The  author  pointed  out  forcibly  the  errors  and  fallacies 
of  previous  writers.  He  stated  that  "Particles  of  food  retained  in 
fissures  and  imperfections  of  the  teeth  and  in  the  spaces  between  the 
teeth  undergo  a  process  of  decomposition  and  acquire  the  property 
of  corroding,  disuniting,  and  therefore  destroying  the  earthy  and 
animal  substances  of  which  the  teeth  are  composed." 

John  Tomes,  a  little  later,  was  the  first  to  record  microscopic 
examinations  of  carious  dentin.    He  described  the  transparent  zone 

1  International  Dental  Journal,  1884. 

2  For  an  interesting  and  exhaustive  exposition  of  their  views,  see  American  System 
of  Dentistry,  Section  on  Dental  Pathology,  by  Black. 

3  A  Practical  Treatise  on  the  Human  Teeth,  second  edition,  Philadelphia,  1839. 

22  ■  ( 337 ) 


338  DENTAL  CARIES 

lying  between  the  carious  and  non-carious  dentin,  and  observed  and 
pointed  out  also  the  dentinal  fibrillee.  He  announced  the  very 
significant  fact  in  relation  to  caries,  that  if  blue  litmus  paper  be 
applied  to  a  carious  cavity  it  is  at  once  reddened,  which  furnishes 
evidence  of  the  presence  of  an  agent  capable,  if  unresisted  by  the 
vitality  of  the  dentin,  of  depriving  the  tissue  of  its  earthy  constitu- 
ents, leaving  the  "gelatin  to  undergo  a  gradual  decomposition 
favored  by  the  heat  and  moisture  of  the  mouth. 

Tomes  first  established  the  essentially  chemical  character  of  some 
features  of  caries.  The  character  of  the  acid  and  its  localization  were, 
however,  not  ascertained. 

In  1867  Bridgman  promulgated  the  theory  that  the  crown  of  the 
tooth  and  the  gum  were  of  different  electrical  potential,  and  that 
being  bathed  in  the  oral  fluids,  the  conditions  of  a  battery  were  set  up. 

Acid  substances  were  said  to  be  set  free  at  the  positive  pole  (the 
crown),  causing  decalcification. 

S.  B.  Palmer,  in  1874,  claimed  that  after  filling,  recurrent  caries  was 
caused  by  the  conditions  of  a  battery  being  set  up — i.  e.,  the  differ- 
ence of  electrical  potential  between  the  filling  and  dentin  in  the 
presence  of  saliva  or  of  the  fluid  of  the  dentin,  as  an  electrolyte 
caused  liberation  of  acids,  producing  decalcification  of  the  tooth  or 
disintegration  of  the  filling — e.  g.,  oxyphosphate. 

Miller,  in  1881  and  1900,^  experimentally  examined  these  assump- 
tions. He  ground  the  enamel  away  from  the  crowns  of  freshly 
extracted  teeth  and  filled  cavities  made  in  them  with  gold  and  gutta- 
percha. These  he  placed  in  separate  flasks  containing  a  physiological 
salt  solution  (0.75  per  cent,  sodium  chlorid).  This,  in  the  presence 
of  electric  currents,  should  produce  hydrochloric  acid  by  liberation  of 
hydrogen  and  chlorin,  and  decalcification  should  occur.  After  four 
years  there  was  no  decalcification. 

Similarly  filled  teeth  were  suspended  in  dilute  lactic  acid.  The 
decalcification  was  exactly  similar  to  that  in  the  unfilled  pieces  used 
as  a  control.  Had  electrolytic  currents  been  generated  between  the 
metals  and  dentin,  the  latter  would  have  been  acted  upon  more 
vigorously  than  in  the  unfilled  pieces. 

In  1868  Watt^  advanced  the  theory  that  free  sulphuric,  nitric,  and 
hydrochloric  acids  were  generated  in  the  mouth  during  putrefactive 
processes  and  caused  the  different  varieties  of  caries. 

Magitot^  pointed  out  that  the  essential  phenomena  of  caries,  as 
they  were  then  understood,  were  the  same  in  natural  teeth  mounted 
upon  plates  as  in  the  natural  organs  in  situ;  proving  that  caries  is 

1  Dental  Cosmos,  April,   1901.  =  Chemical  Essays,   1868. 

3  Treatise  on  Dental  Caries,  Experimental  and  Therapeutical  Investigations. 


EXCITING  CAUSES  339 

intrinsically  independent  of  existence  of  vitality.  By  immersing 
teeth  in  solutions  of  sugar  undergoing  fermentative  changes,  he  found 
that  decalcification  occurred.  Teeth  immersed  in  solutions  of  sugar, 
in  which  fermentation  had  been  prevented  by  boiling  the  solution 
and  sealing,  or  by  additions  of  sufficient  carbolic  acid,  remained 
unaffected. 

Leber  and  Rottenstein,  in  1867,  first  called  attention  to  the 
probable  causative  association  of  bacteria  with  some  phases  of 
dental  caries.  By  staining  carious  dentin  with  iodin,  the  dilated 
dentinal  tubules  were  shown  to  be  filled  with  granular  bodies,  which 
they  recognized  as  bacteria,  identifying  but  one  of  the  many  forms 
of  oral  bacteria — 'the  leptothrix.  They  deemed  an  initial  exposure  of 
dentin  a  necessary  preliminary  to  the  invasion  and  growth  of  the 
leptothrix,  which  in  conditions  of  lessened  resistance  gained  access  to 
the  tubules  and  in  some  undescribed  manner  caused  their  dilatation. 

The  question  of  the  recognition  of  the  presence  of  bacteria  directly 
resolves  itself  into  the  subject  of  special  staining.  Prior  to  the  work 
of  Koch,  presented  in  1881,  no  means  of  isolating  specific  bacteria 
by  special  cultures  and  staining  were  known,  and  it  is  remarkable 
that  in  the  same  year,  the  essential  features  of  dental  caries  were 
first  made  out  with  some  degree  of  clearness. 

Miles  and  Underwood  (World's  Medical  Congress,  1881)  pointed 
out  clearly  and  at  length,  the  different  appearances  produced  by 
simple  decalcification  of  dentin  and  those  by  dental  caries.  Speak- 
ing of  Magitot's  experiments,  they  say:  "We  assume  that  two 
factors  have  always  been  in  operation:  (1)  The  action  of  acids  and 
(2)  the  action  of  germs.  When  caries  occurs  in  mouths  it  is  always 
under  circumstances  more  favorable  to  the  action  of  germs  than  to 
the  action  of  acids."  They  believed  that  the  acids  necessary  for 
the  decalcification  were  excreted  by  the  germs,  which  utilized  the 
dentinal  fibrillse  as  a  food  supply. 

It  will  be  seen  that  the  invasion  and  multiplication  of  organisms  in 
the  tubuli  were  held  as  the  antecedent  of  the  process  of  decalcifica- 
tion. The  deductions  of  these  observers  were  drawn  from  data 
not  derived  from  the  methods  of  modern  bacteriology — i.  e.,  special 
stains  and  special  cultures.  Moreover,  they  were  made  before  the 
physiological  chemistry  of  bacteria  was  even  partially  understood. 

In  1882  W.  D.  Miller,  of  Berlin,  announced,  as  the  results  of 
experiments  conducted  by  him,  that  he  believed  the  first  stage  of 
dental  caries  to  consist  of  a  decalcification  of  the  tissues  of  the  teeth 
by  acids  which  are  for  the  greater  part  generated  in  the  mouth  through 
fermentation  of  carbohydrate  food  by  bacteria.  This,  it  will  be 
seen,  is  a  position  in  agreement  with  that  of  Robertson. 

The    observations    of    Miller    were    supplemented    by    J.    Leon 


340  DENTAL  CARIES 

Williams,  who  demonstrated  a  microbic  collection  upon  the 
surface  of  superficially  decayed  enamel,  and  having  sufficient 
attachment  to  permit  grinding  in  situ.  Williams  claimed  that 
these  plaques  are  the  primary  agents  which  manufacture  acid  from 
carbohydrate  material  in  association  with  them. 

These,  and  other  observers  whose  names  will  be  mentioned  in 
place,  have  thrown  side-lights  upon  the  formation  and  nature  of  the 
plaque  and  upon  the  pabulum  which  they  require  and  out  of  which 
they  form  acid  as  one  of  their  by-products. 

The  reader  will  be  assisted  in  considering  the  somewhat  discon- 
nected facts  hereafter  given  by  bearing  in  mind  the  generally  accepted 
theory  of  the  modus  operandi  of  caries  deduced  from  the  facts  brought 
out  and  which  is  now  briefly  stated.  The  primary  cause  of  dental 
caries  is  a  collection  of  bacteria  upon  the  surface  of  the  tooth.  This 
probably  begins  with  a  coating  of  the  tooth  by  saliva  in  which  a 
certain  proportion  of  solid  organic  matter  exists — mucin,  globulin, 
leukocytes,  epithelial  scales,  etc. 

This  is  immediately  infected  by  ever-present  bacteria,  which  form 
colonies  in  it.  This  mass  of  organic  basis  and  bacterial  colonies 
when  firmly  established  can  be  ground  in  situ  and  constitute  a 
"microbic  plaque."  By  itself  this  cannot  produce  dental  caries. 
To  this  microbic  plaque  comes  the  carbohydrate  food  which  is  the 
second  essential  factor  in  caries. 

This  carbohydrate  is  changed  by  the  bacteria  to  acid,  mainly  lactic 
acid.  This  decalcifies  the  tooth  substance,  leaving  the  organic  matrix. 
The  organic  matrix  is  next  destroyed  by  bacteria  having  the  power 
of  its  liquefaction,  probably  due  to  their  enzymes.  Both  the  inorganic 
and  organic  bases  of  tooth  structure  being  destroyed,  a  cavity  is  left. 
This  being  a  relatively  slow  process,  the  intermediate  stages  are  found. 

There  was  exception  taken  to  this  theory  by  Miller,  who  claimed 
that  plaque  formation  was  not  essential,  but  that  the  infected  food 
mass  could  form  the  acid  and  act  directly.  This  is  simply  a  question 
of  whether  bacteria  act  in  the  mass  or  under  the  mass,  and  is  only 
a  question  of  modus  operandi,  not  of  essential  fact.  PickerilP  endorses 
Miller's  viewpoint,  but  so  far  as  the  writer  is  aware  neither  Miller  nor 
Pickerill  have  offered  any  satisfactory  proof  that  the  plaque  which 
von  Beiist  has  shown  to  form  in  a  few  hours  is  not  the  localizing 
factor.  There  is,  indeed,  no  reason  why  an  infected  food  mass  should 
not  form  its  own  underlying  plaque  out  of  there  existing  mucin  and 
bacteria.  The  theory  of  self  solution  of  base  of  attachment  of  the 
plaque  (reason  2^)  seems  weak  in  view  of  the  rapidity  of  bacterial 
reproduction. 

1  The  Prevention  of  Dental  Caries  and  Oral  Sepsis,  2d  Ed.,  p.  24.  2  ibid. 


EXCITING  CAUSES  341 

Miller's  observations  and  experiments  established  the  following 
basal  facts  in  connection  with  dental  caries: 

1.  That  in  all  cases  of  dental  caries  microorganisms  may  be  seen 
under  the  microscope  in  the  tubules  of  the  carious  dentin,  and  that 
bacteria  exist  in  great  numbers  in  the  mouth. 

2.  That  the  invasion  of  the  tubules  is  always  preceded  by  decal- 
cification of  the  dentin — i.  e.,  an  area,  sometimes  relatively  large, 
of  decalcified  dentin  may  be  seen  in  advance  of  the  organisms. 

3.  Analysis  of  the  softened  dentin  proved  that  a  large  part  of  its 
lime  salts  were  removed — i.  e.,  decalcification  had  occurred. 

4.  Test  with  litmus  paper  gave  the -acid  reaction  in"  nearly  every 
case,  so  that  the  inference  that  decalcification  was  due  to  an  acid 
was  warrantable. 

5.  The  food  substances  taken  into  the  mouth  are  of  all  classes. 
Carbohydrates  (sugars  and  starches),  hydrocarbons  (fats),  and 
nitrogenous  (albuminous)  materials. 

The  carbohydrates  are  fermented  with  acid  reaction  by  many 
•mouth  bacteria,  commonly  producing  lactic  acid;  the  albumins 
ferment  with  an  alkaline  reaction. 

It  was  inferred  from  this  and  other  experiments  that  caries  was 
due  to  the  acid  fermentation  of  carbohydrates  and  not  directly  to 
the  fermentation  of  albuminous  substances. 

6.  That  oral  fermentation  is  the  result  of  bacterial  action,  his 
following  fundamental  experiments  show: 

(a)  A  small  tube  was  filled  with  a  solution  of  starch  and  fastened 
to  a  molar  tooth  on  retiring.  The  next  morning  the  contents  of  the 
tube  had  a  strong  acid  reaction.  A  tube  of  the  starch  solution  with 
saliva  added  was  incubated  at  blood  temperature.  After  four  or 
five  hours  the  mixture  became  acid. 

(6)  The  mixture  of  starch  and  saliva  was  kept  at  100°  C.  for  a  half- 
hour,  and  incubated.  It  did  not  become  acid — i.  e.,  the  exposure  to 
this  temperature  killed  the  ferment." 

(c)  The  saliva  was  boiled  for  a  half  hour  and  then  added  to  the 
starch  solution  and  the  mixture  incubated'.  No  acid  w^as  produced — 
i.  e.,  the  ferment  existed  in  the  saliva,  not  in  the  starch. 

{d)  The  ptyalin  of  the  saliva  was  destroyed  by  heating  the  mixture 
for  twenty  minutes  at  67°  C;  the  incubated  mixture  still  became 
acid — i.  e.,  ptyalin  did  not  act  as  the  acid-forming  ferment,  but  the 
fermentation  must  have  been  caused  by  some  other  ferment  not 
destroyed  by  exposure  to  this  temperature. 

(e)  To  the  mixture  of  saliva  and  starch,  carbolic  acid  was  added 
as  an  antiseptic.  No  acid  was  formed,  but  the  ptyalin  changed  the 
starch  to  sugar — i.  e.,  the  acid-forming  bacteria  were  inhibited,  the 
ptyalin  not. 


342  DENTAL  CARIES 

(/)  A  number  of  tubes  were  each  supplied  with  a  small  quantity  of 
the  saliva-starch  solution  and  sterilized;  a  third  of  them  were  infected 
from  the  mouth,  a  third  by  carious  dentin,  and  a  third  were  left 
uninfected  as  controls.  The  infected  tubes  became  acid;  the  controls 
did  not. 

(g)  The  first  of  a  series  of  tubes  containing  sterilized  saliva  and 
starch  solution  was  infected  with  carious  dentin;  when  this  became 
acid  a  fraction  of  a  drop  was  carried  from  it  to  a  second  tube.  After 
that  became  acid  a  third  was  infected  from  it,  and  so  on  indefinitely. 

Conclusion. — Carious  dentin  contains  a  ferment  or  ferments  cap- 
able of  reproduction — i.  e.,  living  organisms  are  present  in  it. 

7.  The  nature  of  this  living  ferment  was  determined  by  infecting 
a  culture  medium  with  carious  dentin  taken  from  the  deeper  layers. 
The  bacteria  cultivated  were  distended  into  pure  cultures  by  carry- 
ing through  a  series  of  cultures  and  examining  microscopically  during 
the  process.  The  same  morphological  characteristics  were  exhibited 
in  the  last  tube,  as  shown  by  the  germs  in  the  deeper  layers  of  carious 
dentin  itself,  and  were  identical  with  that  of  Bacterium  acidi  lactici. 
These  germs  may  be  found  in  the  sediment  of  a  culture  tube,  and 
consist  of  cocci  and  micrococci,  either  single  or  in  chains.  These 
cocci  possess  the  power  of  forming  lactic  acid  from  glucose.  The 
organism  is  a  faculatative  anaerobe  (Fig.  319). 

8.  A  sound  bicuspid  was  sawed  into  sections,  and  an  equal  number 
of  these  sections  placed  in  each  of  two  test-tubes.  Upon  these  was 
poured  a  2  per  cent,  aqueous  extract  of  beef  (albuminous).  To  one 
tube  a  minute  portion  (0.2  per  cent.)  of  cane-sugar  was  added.  Both 
tubes  were  sterilized,  and  after  cooling  infected  with  a  pure  culture 
of  the  germ,  obtained  from  the  deeper  layer  of  carious  dentin.  The 
sugar-containing  solution  became  acid  in  a  few  hours;  in  a  week  the 
dentin  was  softened;  in  two  weeks  thin  sections  were  completely 
decalcified ;  in  three  weeks  cavities  were  found  in  the  dentin,  exactly 
similar  to  cavities  formed  in  teeth  in  the  mouth  and  presenting  under 
the  microscope  other  phenomena  of  caries  to  be  described  later. 

A  more  prolonged  fermentation  resulted  in  the  complete  disintegra- 
tion of  the  slabs  of  dentin,  a  proof  of  the  fact  that  one  organism  may 
completely  destroy  dentin. 

In  the  tube  containing  only  the  extract  of  beef,  no  acid  was  pro- 
duced, and  no  decalcification  of  the  dentin  occurred. 

From  these  facts.  Miller  argued  that  putrefaction  does  not  initiate 
the  process  of  dental  caries,  and  may  not  be  essential  to  the  destruc- 
tion of  either  the  inorganic  or  organic  dental  elements. 

9.  That  the  acid  produced  was  lactic  acid,  Miller  demonstrated 
as  follows: 


EXCITING  CAUSES 


343 


Starch  and  saliva  were  mixed  and  fermentation  induced.  This 
was  then  checked  by  steriHzation  with  heat.  A  quantity  of  material 
being  collected  in  this  manner,  the  whole  was  concentrated  by 
evaporation,  and  tested  with  a  solution  of  methyl  violet,  which 
would  turn  first  blue  and  then  green  with  an  inorganic  acid.  Not 
so  reacting,  and  not  distilling  off  during  the  concentration,  the  acid 
present  was  pronounced  a  non-volatile  organic  acid.  The  concen- 
trate was  shaken  with  a  quantity  of  ether,  which  dissolved  the  organic 
acid  present.  When  the  solution  was  clear,  it  was  filtered  and  the 
ether  partially  distilled  off,  when  the  partially  concentrated  solution 
was  further  concentrated  over  a  water  bath  and  then  mixed  with  an 
excess  of  freshly  prepared  zinc  oxid.  The  whole  was  boiled,  water 
being  added  as  needed,  until  the  solution  became  neutral,  when  it 
was  set  aside  to  crystallize.  A  drop  placed  upon  a  slide  under  the 
microscope  showed  the  forms  of  crystals  of  zinc  lactate  (Fig.  320). 


Fig.  319 


Fig.  320 


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0 


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By  testing  the  molecular  weight  of  the  washed  and  dried  crystals, 
it  was  determined  clearly  that  the  substance  was  zinc  lactate. 

In  practically  a  similar  manner,  lactic  acid  was  obtained  directly 
from  carious  dentin. 

While  Miller  demonstrated  the  ability  of  one  organism  to  produce 
all  the  essential  phenomena  of  caries,  including  liquefaction  of  the 
dentin,  he  did  not  claim  that  only  one  or  two  organisms  are  involved 
in  the  process,  but  that  "any  germs  possessing  the  power  of  producing 
acid  fermentation  of  food  may  and  do  take  part  in  the  first  stage  of 
caries,  and  that  all  those  possessing  a  peptonizing  or  digestive  action 
upon  albuminous  substances  may  take  part  in  the  second  stage; 
and  that  those  possessing  both  properties  may  take  part  in  both 
stages."^ 

1  Microorganisms  of  the  Human  Mouth. 


344  DENTAL  CARIES 

He  was  of  the  opinion  that  it  is  not  the  presence  of  this  or  that 
kind  of  bacterium,  but  rather  the  joint  activity  of  the  total  flora, 
as  expressed  in  intensity  of  fermentation  in  food  particles,  which 
determines  the  extent  of  caries. 

Out  of  eighteen  mouth  bacteria  examined,  Miller  found  ten  that 
produced  lactic  acid  in  sugar-containing  solutions.^  He  also  found 
acetic  and  butyric  acid  to  be  by-products.  Miller  and  others  have 
found  lactic-acid-producingbacteria  plentiful  in  the  mouthsof  immune. 

Hinkins  and  Acree,^  in  experiments  upon  pure  cultures  of  a  number 
of  oral  bacteria  in  various  artificial  media,  found  lactic,  butyric, 
valerianic,  formic,  carbonic,  and  hydrosulphuric  acids  as  either 
principal  or  by-products  of  the  fermentation. 

It  is  quite  clear  from  Miller's  demonstrations  that  bacteria,  or 
at  least  one  bacterium,  are  the  exciting  causes  of  dental  caries;  and 
that  for  their  function  as  such  they  require  carbohydrate  material  as 
food.  It  is  probably  true  that  in  order  to  act,  the  acid-producing 
bacteria  must  be  attached  to  the  teeth  in  the  form  of  plaques  (to  be 
later  described) ,  or  the  food  and  bacteria  as  a  mass  must  be  attached 
at  some  undisturbed  location. 

The  action  of  bacteria  upon  these  substances  has  been  studied.  The 
carbohydrates  introduced  into  the  mouth  as  food  are  monosac- 
charids,  disaccharids,  and  polysaccharids.  (1)  The  monosaccharids 
or  glucoses  have  the  general  formula  C6H12O6,  and  are  represented  by 
dextrose  and  levulose,  found  in  seeds,  fruits,  roots,  honey,  and  in 
many  forms  of  candy,  such  as  peanut  brittle  and  glace s,  and  galac- 
tose formed  from  lactose  or  milk  sugar  by  hydrolysis.  These  ferment 
directly  into  lactic  acid  without  formation  of  gas. 

C6H12O6  +  bacterial  enzyme  =  2C3H6O3. 

A  certain  proportion  of  the  glucose,  etc.,  is  appropriated  by  the 
bacteria  as  food.  (2)  Disaccharids  or  saccharoses  have  the  general 
formula  C12H22O11.  The  principal  one  is  saccharose,  found  in  sugar- 
cane, the  sugar-beet,  sugar-maple,  and  maize.  This  is  inverted  by 
the  ferment  of  the  bacteria  into  glucose  and  levulose  through  a 
process  of  hydration: 

C12H22O11  +  H2O  +  bacterial  enzyme  =  C6H12O6  =  C6H12O6. 

Two  other  disaccharids  enter  the  mouth  or  are  formed  therein: 
lactose  and  maltose,  both  C12H22O11  (H2O).  Lactose  exists  in  milk, 
and  by  hydrolysis  is  changed  by  bacteria  to  galactose,  2C6H12O6,  and 
then  ferments  like  other  monosaccharids.  Maltose  is  an  intermediate 
product  in  the  formation  of  glucose  from  starch,  and  is  produced  by 
the  action  of  ptyalin.     It  is  readily  fermentable  by  yeast  and  by 

1  Microorganisms  of  the  Human  Mouth.  ^  Dental  Cosmos,  1901. 


EXCITING  CAUSES  345 

some  mouth  bacteria  (Goadby).  (3)  Polysaccharids  or  amy  loses 
with  the  general  formula  (C6Hio05)n.  Starch,  cellulose,  glycogen,  and 
gum. 

Starch  was  found  by  Miller  not  to  undergo  direct  fermentation  by 
mouth  bacteria — i.  e.,  culture  media  containing  starch,  but  not 
sugar,  when  infected  by  bacteria  did  not  ferment  into  lactic  acid 
unless  ptyalin  was  present.^  When  saliva  was  used,  however,  the 
acid  reaction  occurred,  owing  to  the  formation  of  glucose  through  the 
action  of  ptyalin. 

In  oral  fermentation  starch  is  first  changed  by  ptyalin  to  maltose 

by  hydration,  and  the  maltose  to  glucose.    Then  the  bacteria  change 

this  to  lactic  acid. 

2C6H10O5  +  2H2O  +  ptyalin  =  Ci.2H220n(H20). 
Starch.  Water.  Maltose. 

Erythrodextrin  and  achrodextrin  are  said  to  be  associate  products. 

Ci2H220ii(H20)  +  ptyalin  =  2C6H12O6. 
Maltose,     or  Bacterial  Enzyme. 

2C6H12O6  +  bacterial  enzyme  =  4C3H6O3. 

In  a  serial  of  seven  papers  in  the  American  Dental  Journal,  beginning  November, 
1910,  J.  Oxford  Keller,  D.D.S.,  endeavors  to  establish  the  claim  that  dental  caries  is 
produced  by  causes  existing  in  the  saliva  apart  from  organic  acids  produced  by  micro- 
organisms.    The  causes  ascribed  are: 

1.  Neutral  salts — a  chemical  combination  of  acid  and  base,  as  potassium  phosphate. 

2.  Neutral  salt  acid  or  neutral  salts  with  excess  acidity. 

3.  Neutral  salt  alkaline  or  neutral  salts  with  excess  alkalinity. 

These  by  chemism  are  supposed  to  extract  the  salts  from  tooth  structure. 

After  making  the  assertion  that  lactic  acid  has  never  been  discovered,  even  in  trace, 
in  human  saliva,  he  states  that  such  acids  as  lactic,  sulphuric,  muriatic,  acetic,  oxalic, 
phosphoric,  malic,  and  carbonic  may  be  contained  in  saliva  in  combination  or  associa- 
tion.    (Compare  with  Miller's  determination  of  lactic  acid  in  carious  dentin. — Editor.) 

He  states  that  lactic  acid  does  not  develop  in  the  mouth  in  sufficient  strength  to 
cause  caries;  that  full  digestive  fermentation  necessary  to  produce  lactic  acid  requires 
from  three  to  six  days,  and  any  found  would  be  neutralized  by  the  alkaline  saliva. 
(Compare  with  Miller's  Experiment,  No.  6,  a. — Editor.) 

The  editor  has  carefully  read  these  papers,  but  can  see  no  reason  to  disturb  the 
text  of  this  work  on  their  account,  for  the  reasons  that: 

1.  The  micro bic  plaques  are  always  present  in  enamel  in  incipient  decay,  and  should 
protect  against  the  access  of  saliva  to  enamel.  Certainly  it  would  have  to  contend 
with  them,  but  when  the  carbohydrate  element  in  it  is  considered,  it  is  probable  it 
furnishes  them  their  pabulum. 

2.  That  acid  may  exist  in  a  cavity  while  the  saliva  is  alkaline,  and  can  be  often 
noted  in  food  masses  collected  on  teeth,  and  can  be  demonstrated  to  patients  by  the 
aid  of  litmus  paper. 

3.  That  caries  is  clinically  noted  in  the  exact  locations  in  which  plaques  are  found  is 
demonstrable  with  tincture  of  iodin,  whereas  if  salivary  salts  are  alone  responsible 
there  is  no  reason  why  clean  spots  should  not  be  affected. 

4.  That  where  saliva  is  most  abundant,  decay  occurs  least,  as  a  rule. 

5.  Because  the  author  has  by  no  means  shown  how  the  salts  of  saliva  produce 
decay,  as  his  experiments  with  concentrated  saliva,  which  disintegrated  teeth  after 
two  or  three  years  may  have  contained  concentrated  acid,  and  as  compared  with 
Miller's  experiment  No.  8,  seems  unconvincing. 

6.  Black  has  shown  that  the  plaques  formed  by  saliva  in  formation  of  calculus  are 
the  habitat  of  bacteria  after  twenty-four  hours,  hence  their  agency  is  hard  to  exclude. 
(See  p.  349.)    

1  American  System  of  Dentistry,  vol.  i,  p.  805. 


346  DENTAL  CARIES 

According  to  Goadby^  a  few  bacteria  found  in  the  mouth  can  pro- 
duce the  change  direct  from  starch  to  maltose  and  thence  to  acid. 
This  is  of  no  practical  consequence,  however,  as  ptyalin  is  always 
present  in  the  mouth.     (See  Miller  above.) 

Glycogen,  CeHioOs,  or  animal  starch,  is  fermented  to  glucose  by 
liver  cell  ferment,  and  probably  exists  in  the  oral  epithelium,  in 
certain  states  as  well  as  in  the  saliva  in  others,  hence  a  systemic  state 
may  introduce  glucose  (in  diabetes).  (See  Glycogenic  Infiltration 
and  pages  355,  358,  and  359.) 

Miller  has  demonstrated  that  bacteria  produce  acid  from  starches 
and  sugars  in  about  equal  proportions,  provided  the  starches  are 
cooked.  The  cooking  of  starchy  foods  bursts  the  starch  granules 
and  renders  them  more  adhesive  to  the  teeth,  as  well  as  more  fer- 
mentable. The  following  synopsis  of  experiments^  made  with  food 
mixed  with  saliva  in  definite  quantities  speaks  for  itself: 


Duration  of 
Material.  experiment.  Acids  formed  in  units.' 

Bread,  starch,    potato,   macaroni, 

rice,     corn,     and    other    cooked 

starches 12  and  30  hours.     20  to  25  and  42  to  110 

Raw  starches,  potato,  spinach,  etc.  12  and  30  hours.  0  0 

Cane-sugar  and  grape-sugar       .  12  and  30  hours.     17  to  20  and  37  to  41 

Meats,  fish,  eggs,  etc.       ...  12  and  30  hours.  0  or  alkaline. 


The  table  shows  that  albuminous  materials  and  raw  starches 
produce  no  acid  and  are  not  concerned  in  caries  except  in  so  far  as 
meats,  etc.,  act  as  culture  media  perpetuating  bacteria,  which  later 
may  produce  an  acid  reaction  in  carbohydrate  materials. 

Milk  contains  a  carbohydrate  (lactose)  and  often  lactic  acid  bacilli. 
It  therefore  may  supply  both  the  bacilli  and  their  food.  This, 
however,  has  relation  to  caries  only  after  plaque  formation,  or  by 
retention  of  acid  milk  against  the  teeth.  That  such  a  result  may 
occur  has  been  shown  by  Bennett. 

Pickerill^  tested  the  acid-forming  powers  of  foodstuffs,  chewed,  and 
incubated  for  four  days.    The  following  table  resulted : 


1  Mycology  of  the  Mouth. 

2  Microorganisms  of  the  Human  Mouth. 

3  An  acid  unit  equals  the  amount  of  acid  necessary  to  neutralize  0.1  c.c.  of  a  0.5  per 
cent,  solution  of  potassium  hydrate — e.  g.,  if  in  a  quantity  of  acid  material  containing 
an  unknown  amount  of  acid,  25  of  such  alkaline  units  are  necessary  to  neutralize  the 
reaction,  there  were  25  acid  units  present  in  it.  For  purpose  of  comparison  the  quanti- 
ties of  material  used  were  4.0  c.c.  of  saliva  and  0.5  grams  of  the  food. 

■•  The  Prevention  of  Dental  Caries  and  Oral  Sepsis. 


EXCITING  CAUSES  347 

Acid  units  each 
neutralizing  c.c.  of  N/5 
Food  material.  NaOH. 

Pastry 5.2 

White  bread 4.4 

Toast 4.4 

Brown  bread 3.6 

Chocolate 3.6 

Biscuit 3.5 

Apple 2.6 

Potato 2.5 

Bread  and  butter  with  jam 2.5 

Crust  of  bread       . 2.0 

Parsnip .1.7 

Orange 1.2 

Salad ,     ...  1.1 

Cane-sugar 0.9 

Rice 0.9 

Meat  (alkaline  to  acid  unit  N/5H2SO4)      ....     4.8  alkaline 

He  calls  attention  to  the  various  factors  of  viscosity  of  saliva, 
natural  adhesiveness  of  food  to  teeth,  etc.,  as  modifying  factors  in 
inception  of  caries. 

Dr.  Harold  Clark^  has  called  attention  to  the  fact  that  the  English, 
whose  teeth  are  much  subject  to  caries,  consume  chocolate  in  large 
quantities.  The  observation  of  Dr.  Albert  King  (p.  348)  regarding 
white  bread  seems  partly  confirmed. 

The  fats  may  be  fermented  with  production  of  fatty  acids.  Goadby 
has  found  these  of  no  importance  in  relation  to  caries,  but  Miller  has 
shown  that  the  acids  found  in  dermoid  cysts,  among  which  are  fatty 
acids,  can  produce  decalcification;  as  other  acids  were  present,  the 
relation  of  fatty  acids  is  not  quite  clear.  Miller  asserts  that  fats 
deposited  upon  the  teeth,  as  well  as  calculus  retard  decay,  and  that 
fat  mixed  with  saliva  will  give  an  alkaline  reaction.^ 

That  alkalies  do  not  produce  tooth  disintegration  in  the  mouth  is 
shown  by  the  fact  that  a  tooth  is  not  affected  by  alkaline  solutions, 
which  are  not  strong  enough  to  injure  the  soft  parts. 

The  influence  of  carbohydrate  diet  in  the  production  of  caries  is 
well  shown  by  tables  compiled  by  Mummery  and  quoted  by  Miller.^ 
The  races  consuming  a  fish  and  meat  diet  almost  exclusively — e.  g., 
the  Esquimaux — are  recorded  as  having  about  3  per  cent,  of  caries 
in  skulls  examined,  while  those  using  a  mixed  or  vegetable  diet  have 
from  10  to  40  per  cent,  of  caries.  A  most  convincing  example  is 
that  given  by  Miller  of  two  related  tribes  living  on  either  side  of 
the  Andes,  in  the  Argentine  Republic,  and  Chili  respectively.  The 
former,  a  cattle  breeding  and  meat  eating  tribe,  were  practically  free 
from  caries,  while  the  latter,  living  on  mixed  foods,  and  consuming 
sugar,  had  19  per  cent,  of  caries.  Miller  and  others  have  shown  that 

1  Private  communication.  2  Dental  Cosmos,  1904. 

^  Microorganisms  of  the  Human  Mouth. 


348  DENTAL  CARIES 

millers  and  confectioners  rapidly  develop  caries  after  engaging  in 
the  occupation,  probably  owing  to  the  inhalation  of  flour  and  sugar 
dust.  Albert  B.  King^  has  recorded  observations  upon  132  cases  of 
bread  eaters,  finding  that  87  who  used  bakers'  bread  exclusively  had 
much  caries,  31  who  used  alternately  bakers'  and  home-made  bread 
had  a  less  prevalence,  while  the  14  using  home-made  bread  exclusively 
had  only  six  cavities  in  three  years.  The  results  are  certainly  worthy 
of  attention  and  of  further  observations. 

While  the  fermentation  of  carbohydrate  food  debris  into  acid  is 
conceded  to  be  the  active  exciting  cause  of  dental  caries,  the  modus 
operandi  of  the  inception  has  not  been  satisfactorily  settled.  Miller 
held  that  as  he  was  able  to  find  bacterial  plaques  upon  many  sur- 
faces of  teeth,  even  in  the  mouths  of  immunes,  without  caries  beneath, 
the  plaques  had  no  relation  to  the  inception  of  caries  of  enamel,  but 
that  the  carbohydrate  food  collecting  at  favoring  spots  undergoes 
acid  fermentation,  with  production  of  enamel  decalcification,  after 
which  the  bacteria  enter.  By  experiments,  he  determined  that  the 
plaques  rather  hindered  the  action  of  acids  experimentally  used  as  a 
decalcifying  agent.  Black,  on  the  other  hand,  claims  that  the  bacteria 
produce  a  gelatinoid  material  and  are  left  upon  the  teeth  in  the 
form  of  a  plaque  or  zooglea  mass,  and  that  the  plaque  is  a  thin, 
transparent,  slightly  yellowish  film,  not  seen  without  close  inspection. 
(It  can  be  stained  by  iodin. — Editor.)  Williams  found  a  film  of 
bacteria  over  the  decalcified  area  in  almost  all  cases  of  superficial 
caries  of  enamel,  and  that  it  has  sufficient  resistance  to  permit 
grinding  in  situ  (Figs.  336  and  337). 

Goadby  frequently  found  on  the  opaque  white  patches  of  softened 
enamel,  a  coccus  to  which  Williams  called  attention,  which  would 
cause  a  plaque  deposition  upon  teeth  suspended  in  its  culture,  and 
that  when  acid-producing  bacteria  were  mixed  with  the  coccus  and  a 
carbohydrate  medium  used,  superficial  decalcification  of  the  enamel 
under  the  plaques  was  produced  in  from  a  week  to  ten  days. 

Miller  also  showed  that  in  the  immune  with  unclean  teeth,  the 
putrefactive  reaction  was  the  dominant  one,  and  that  the  collection, 
if  persistent,  could  act  as  a  protective  against  the  access  of  acid- 
producing  material. 

In  the  above  data  we  find  that  the  plaques  are  almost  universal, 
even  on  immune  surfaces  (Miller),  so  that  their  presence  on  a  decal- 
cifying surface  is  probably  true,  as  claimed  by  Williams.  If,  then, 
they  are  a  protection  against  the  acids  produced  from  carbohydrate 
they  should  protect,  but  they  do  not.  Secondly,  experiments  with 
formed  acids  are  not  conclusive,  as  they  may  be  germicidal  and 

1  Dental  Cosmos,  1905. 


PREDISPOSING  CAUSES  349 

the  dead  film  might  be  a  relative  protection  against  decalcification 
by  the  acids.  Thirdly,  the  bacterial  films,  if  containing  acid-pro- 
ducing bacteria,  can  easily  take  up  any  carbohydrate  food  collected 
against  them,  form  acid  from  it,  which  they  then  pass  to  the  enamel 
in  a  nascent  state,  hold  it  against  it,  and  permit  it  to  abstract  the 
calcium  salts,  which  they  then  pass  out  as  lactates,  etc.,  or  allow  to 
remain  in  situ.  This  latter  conclusion  in  the  main  is  the  theory  of 
Black,  and  while  the  decalcifying  ability  of  infected  carbohydrate 
food  without  the  intervention  of  a  definite  previously  formed  plaque 
(but  possibly  by  a  self-formed  one)  is  a  possibility,  it  seems  a  reason- 
able conclusion  to  admit  the  activity  of  the  plaques.  Kirk  has  shown 
that  the  precipitation  of  mucin  from  saliva  rich  in  mucin  content, 
by  lactic  acid  produced  by  lactic  acid  bacilli,  plays  a  part  in  the 
development  of  the  plaques,  or  by  binding  the  bacteria  together 
creates  a  bacterial  plaque.  Von  Beiist^  has  shown  that  within  three 
hours,  a  mucinous  deposit  containing  many  colonies  of  bacteria  which 
rapidly  increase  in  size,  may  be  formed.  He  attributes  to  bacteria, 
a  large  share  in  the  formation  of  calculus  which  is  the  theme  of  his 
paper,  but  it  also  throws  light  on  caries  plaques. 

The  frequent  disturbance  of  the  plaques  by  monthly  cleansings 
(prophylaxis),  also  prevents  dental  caries  in  large  degree,  so  that  they 
must  have  some  relation  to  the  inception,  though  it  is  only  fair  to 
state  that  a  constant  warfare  against  any  species  of  bacteria  doubtless 
vastly  reduces  their  number  in  the  mouth. 

Noyes"^  claims  that  in  well-cared-for  mouths  the  confinement  of 
acid  under  the  plaques  is  great,  while  in  uncared-for  mouths,  though 
much  acid  is  formed,  it  may  be  dissipated  in  the  saliva  and  the  teeth 
not  be  much  attacked.  This  argument,  however,  does  not  take  into 
consideration  the  idea  of  Miller,  that  stagnant  materials  take  on  a 
putrefactive  reaction  after  the  acid  production  is  exhausted  (see 
p.  361). 

The  Predisposing  Causes  of  Caries.— The  causes  of  the  predis- 
position to  caries  are  local  and  general. 

Local  Predisposing  Causes. — So  invariably  does  caries  begin  in 
sulci  or  pits  upon  approximal  surfaces,  about  defective  fillings,  and 
upon  unclean  surfaces,  that  faults  of  form  or  retentive  nature  of 
approximation,  defects,  and  faulty  position  of  the  teeth  must  bear  a 
relation  to  the  difficulty  of  keeping  the  parts  free  from  accumulations 
of  bacteria  and  carbohydrates. 

These  local  predisposing  causes,  as  they  are  called,  are  simply 
conditions  favoring  the  formation  of  the  bacterial  plaques  upon  the 
teeth  and  the  retention  of  carbohydrate  food. 

1  Items  of  Interest  June,  1912.  2  Ibid.,  1909,  p.  750. 


350  DENTAL  CARIES 

Lack  of  Oral  Hygiene. — This  is  perhaps  the  most  frequent  local 
predisponent  of  caries.  It  is,  in  fact,  a  factor  in  the  exciting  cause 
and  its  reverse  is  prophylaxis.  Most  people  either  can  not  or  will 
not  cleanse  the  teeth  thoroughly,  hence  their  lack  of  care  predisposes 
them  to  caries.  It  may  not  occur,  but  is  liable  to  do  so.  Otherwise 
lack  of  hygiene  means  the  presence  of  microbic  plaques  and  carbo- 
hydrate food,  and  these  are  exciting  causes  of  caries. 

Faults  of  Form. — Deep  pits  or  sulci  in  the  occlusal  surfaces  of 
bicuspids  or  the  occlusal  or  buccal  surfaces  of  molars,  or  in  the  lingual 
surfaces  of  incisors,  and  occasionally  cuspids,  or  pits  upon  the  cusps 
of  bicuspids  or  molars,  or  in  other  unusual  situations,  are  not  sub- 
jected to  a  cleansing  friction,  and  so  permit  bacteria  to  form  plaques 
in  these  locations  (Figs.  322  to  335). 

.  The  nature  of  the  approximal  contact  has  to  do  with  the  inception 
of  caries.  Teeth  are  seen  in  which  the  approximal  surfaces  are  well 
rounded  and  their  buccal  and  lingual  angles  free  from  approximation. 
Such  teeth  are  usually  relatively  narrow  at  their  cervices,  so  that 
these  also  recede  well  from  the  line  of  contact.  A  V-shaped  space 
is  formed,  which  the  gum  festoon  normally  nearly  fills.  Such  per- 
fection of  contour  is  also,  as  a  rule,  associated  with  a  perfect  organi- 
zation of  the  enamel  structure,  in  virtue  of  which  the  surface  is 
smooth.  While  such  teeth  may  decay  approximally,  there  is  much 
less  tendency  to  caries  (Fig.  338). 

Opposed  to  this,  approximations  exist  of  a  broad  nature.  Broad 
approximations  are  very  common,  and  not  infrequently  are  asso- 
ciated with  a  certain  degree  of  enamel  opacity  and  an  unevenness 
of  enamel  surface  plainly  visible  to  the  naked  eye  (see  p.  352). 

The  fluid  exuded  by  the  gum  is  normally  alkaline  in  character, 
and  probably  neutralizes  the  products  of  acid  fermentation.  In  view 
of  this  fact,  the  first-mentioned  form  of  contact  evidently  affords 
more  of  this  immunizing  principle.  The  extension  of  cavity  margins 
beneath  the  gum  has  been  strongly  indicated  by  experience  as  good 
practice,  and  probably  is  explainable  upon  the  same  ground.  There 
is  also  some  evidence  that  the  gum  has  some  cleansing  action  (prob- 
ably phagocytic)  upon  metal  placed  beneath  it,  as  it  is  noted  that 
when  unclean  gold  crowns  are  removed  the  portion  extending  beneath 
the  gum  is  usually  quite  clean. 

With  the  narrow  approximations,  saliva  is  readily  forced  between 
the  teeth  and  neutralizes  the  acids  formed,  or  washes  away  soluble 
carbohydrates,  the  food  for  the  bacteria.  With  the  broad  approxima- 
tions such  a  result  is  less  likely  to  occur. 

Stagnant  saliva  retaining  carbohydrates,  probably  will  develop  an 
acid  reaction.    (Miller.) 


PREDISPOSING  CAUSES  351 

A  depressed  approximal  surface  may  decay,  but  frequently  does 
not.    An  acquired  fault  of  form  requires  notice. 

Anatomically,  the  gum  covers  the  cementum  and  the  enamel 
margin.  When  recession  of  the  gum  occurs,  the  cementum  is  left 
exposed  and  food  debris  accumulates  at  the  angle  formed  by  it  with 
the  gum.  Owing  to  the  cementum  being  less  smooth  than  enamel, 
microbic  plaques  readily  collect,  hence  decay  of  the  cementum 
frequently  occurs,  and  is  apt  to  progress  rapidly,  owing  to  the 
natural  low  percentage  of  inorganic  matter  (Figs.  321,  332,  and  364). 

Arrangement  and  Position  of  the  Teeth. — The  overlapping 
of  one  tooth  upon  another  creates  a  form  of  contact,  producing  a 
tendency  to  decay  at  that  point.  Angle^  claims  to  have  observed  a 
comparative  freedom  from  caries  of  very  irregular  teeth  (Fig.  335). 

The  presence  of  a  supernumerary  third  molar,  lying  at  the  buccal 
side  of  the  interdental  space,  between  the  second  and  third  upper 
molar,  or  an  inlocked  bicuspid,  very  frequently  causes  approximal 
caries  at  the  contact  points.  The  upper  third  and  lower  third  molars 
frequently  stand  in  bad  relation  to  the  cheek  or  the  gum. 

Food  collects  upon  their  buccal  surfaces,  or  they  are  not  subjected 
to  the  friction  of  the  tooth-brush,  and  decalcification  of  a  broad  area 
of  a  buccal  surface  frequently  results. 

Defects  about  Fillings. — Under  the  caption  of  Recurrence  of 
Caries,  will  be  found  a  list  of  the  causes  which  perpetuate  caries  about 
fillings.  Defectively  cemented  bands  are  also  a  cause.  I  believe 
the  abundance  of  these  and  a  lack  of  oral  hygiene  to  be,  in  a  large 
degree,  the  measure  of  a  tendency  to  persistent  caries.  A  patient 
has  a  large  number  of  cavities  due  to  a  period  of  negligence,  with 
consequent  intensity  of  oral  fermentation.  If  these  are  obliterated 
in  the  best  manner  with  physically  perfect  fillings,  and  oral  hygiene 
be  exact,  the  tendency  to  caries  is  largely  obliterated.  If,  on  the 
other  hand,  a  large  number  of  even  slightly  defective  fillings  are 
made,  not  only  is  recurrent  caries  induced,  but  the  caries  ferment  is 
continuously  active,  and  exact  oral  hygiene  is  an  impossibility.  The 
number  of  cleansings  a  day  is  no  guarantee  of  perfect  hygiene,  even 
with  perfect  teeth,  as  nothing  is  more  common  than  to  see  unclean 
embrasures  easily  taking  the  stain  of  tincture  of  iodin  even  in  the 
anterior  part  of  the  mouth  (in  less  degree  than  shown  in  Fig.  321). 
Unquestionably,  food  debris  may  even  be  swept  into  the  interdental 
spaces  by  brushing  alone.  Miller^  has  shown  that  a  mixture  of  bread 
and  saliva  may  become  decidedly  acid  in  one  hour,  and  superficially 
decalcify  sections  of  dentin  in  five  hours.    With  this  going  on,  day 

1  Dental  Cosmos,   1903.  2  jbid.,  1905. 


352 


DENTAL  CARIES 


after  day,  in  cases  of  soluble  teeth  and  without  other  aid  than 
brushing,  and  often  this  not  thoroughly  done,  the  persistence  of 
decay  is  not  surprising.  This,  however,  does  not  prove  the  absence 
of  systemic  susceptibility  or  immunity,  as  an  added  cause  of  caries 
or  its  absence.  A  condition  similar  to  a  defect  about  a  filling,  is 
that  of  the  presence  of  an  orthodontic  appliance  which  may  afford 
convenient  nooks  for  caries,  fungi,  and  food.  In  the  use  of  base 
metal  wires  about  teeth  for  pyorrhea,  the  wire  either  has  some  anti- 
septic, action  probably  due  to  the  contained  copper,  or  the  pj^orrhetic 
condition  itself  furnishes  an  alkaline  element.  In  such  case  caries 
frequently  does  not  occur. 

Fig.  321 


Caries  of  enamel  about  the  cervices  of  many  teetli,  due  to  tenacious  films  collected 
upon  them;  at  first  probably  neglected,  later  impossible  to  cleanse  with  brush  alone. 
(Model  by  W.  A.  Capon.)  Fairly  clean  teeth  stained  Yith  iodin  present  such  an  appear- 
ance.    (See  prophylaxis.) 


Structure. — While  the  structure  of  the  enamel  has  no  relation  to 
the  inception  of  caries,  that  is,  teeth  of  poor  structure  may  not 
decay,  a  roughness  of  the  enamel  surface,  which  often  accompanies 
teeth  of  opaque  appearance,  may  act  as  a  favoring  condition, 
and  after  inception  of  caries,  inferior  structure  and  possibly  the 
presence  of  Caush's  tubes  may  permit  more  rapid  disintegration. 
(See  p.  243.)^  An  interesting  examination  of  16,000  mouths,  made  in 
Sweden  by  Forberg  (Stockholm),  and  others  by  Rose  in  Baden  and 
Thuringia  seems  to  show  that  there  is  a  relation  between  the  color 
(structure)  of  teeth  and  the  presence  of  caries,  the  following  averages 

^  This  statement  now  made  in  two  editions  has  been  further  experimentally  con- 
firmed by  Pickerill  (The  Prevention  of  Dental  Caries  and  Oral  Sepsis,  2nd  Ed.),  who 
has  shown  by  rubbing  graphite  upon  the  surface,  what  he  terms  "imbrication  lines," 
which  are  associated  with  "calcarine"  fissures  in  some  teeth.  Those  teeth  which 
contain  many  of  the  lines  and  fissures  are  termed  "malacotic, "  while  those  but 
slightly  imbricated  are  termed  "sclerotic."  By  test,  "malacotic"  teeth  were  found 
more  soluble  in  lactic  acid  solutions  than  the  sclerotic  (Ibid.,  p.  129).  A  similar 
result  was  obtained  with  hydrochloric  acid.  Malacotic  and  sclerotic  teeth  were  both 
but  little  affected  after  insertion  into  an  orange  for  a  week  but  the  malacotic  were  more 
affected  (Ibid.,  p.  130).  This  fact  is  of  importance  in  prophylaxis  (which  see).  Carbon 
dioxid  in  strong  solution  was  found  to   have  no  effect  upon  teeth  (Ibid,  p.  133). 


PREDISPOSING  CAUSES  353 

of  all  ages  being  observed:  White  teeth,  14.3  per  cent,  of  caries; 
yellowish-white,  16.4  per  cent.;  yellow,  20  per  cent.;  grayish  blue, 
24.3  per  cent. 

According  to  these  observers,^  in  the  regions  in  which  the  water 
was  rich  in  calcium  salts  the  individuals  examined  had  the  yellowish- 
white  teeth.    Miller's  observations  confirm  this. 

Gautier^  has  found  that  in  young  pigs,  deficient  osseous  development 
corresponded  exactly  to  the  lack  of  calcium  salts  in  their  drinking 
water. 

Black^  made  analyses  of  so-called  hard  and  soft  teeth,  and  deduced 
from  them  the  opinion  that  the  hardness  and  softness  of  teeth  have 
nothing  to  do  with  the  inception  of  caries. 

Touching  this  point,  Black*  instances  the  case  of  a  man  whose 
enamel  had  always  been  chalky  and  as  easily  cut  as  a  slate-pencil, 
yet  who  had  little  caries  of  the  teeth.  That  some  teeth  of  apparently 
poor  structure  and  defective  form  do  not  decay  is  also  a  fact  of 
common  observation,  but,  as  a  rule,  they  go  together. 

These  observations,  together  with  the  foregoing  data,  regarding 
the  inception  of  caries,  point  to  the  now  conceded  conclusion  that 
the  caries  of  teeth  is  entirely  due  to  the  environment  of  the  teeth, 
and  in  no  sense  does  it  arise  from  within  the  tooth,  and  that  in  so 
far  as  the  cause  is  active,  it  is  a  question  of  the  localization  of  the 
exciting  cause  or  its  factors  on  the  one  hand,  and  the  solubility  of 
the  teeth  on  the  other;  and  that  no  amount  of  cause  is  sufficient  to 
produce  it,  unless  permitted  to  exert  its  effect  upon  special  points 
upon  the  teeth;  in  other  words,  it  requires  localization  and  time  to 
act,  though  it  may  in  some  cases  be  broadly  localized. 

Other  Local  Predisposing  Causes. — ^Acids  taken  in  excess  into 
the  mouth  may  act  as  predisponents  by  causing  a  roughness  of  the 
enamel,  which  invites  the  formation  of  the  bacterial  plaques.  A 
course  of  tincture  of  ferric  chlorid  has  a  bad  reputation  in  this  con- 
nection. In  the  cases  observed  by  the  editor,  the  hydrochloric  acid 
in  the  tincture  seemed  to  have  formed  roughnesses  between  the 
teeth,  and  many  large  cavities  of  not  unusual  form  were  later  pro- 
duced and  evidently  due  to  the  carious  process.  Weld,^  in  a  series 
of  experiments  to  determine  the  action  of  ferric  chlorid,  found  that 
the  pure  tincture  had  little  effect,  while  in  the  dilution  of  1 : 5  in  water 
it  had  much;  destroying  the  entire  enamel  in  twenty-four  hours. 
Head's  observations  on  the  effect  of  dilute  acids  are  in  general  accord 
with  this  principle  (see  p.  314).     This  fact  indicates  the  prompt 

1  Dental  Cosmos,  1911.     -  L'Odontologie,  October,  1910.   See  Cosmos,  1911,  p.  242. 

3  Ibid.,  1898.  •*  Ibid. 

5  Quoted  by  Prentiss,  Dental  Cosmos,  September,  1912,  p.  1006. 

23 


354  DENTAL  CARIES 

local  use  of  an  alkali  after  a  dose.  (See  Prophylaxis  of  Caries.) 
Howe^  claims  that  iron,  whether  as  chlorid  or  carbonate,  taken  in 
capsules,  returns  to  the  salivary  gland  for  excretion  as  ferric  chlorid 
and  may  exert  injurious  effects. 

Morjenstern^  describes  experiments  that  show  that  acid  iron  waters 
or  tinctures  have  a  decalcifying  action,  ferrous  iodid  and  ferric 
chlorid  being  particularly  injurious,  while  reduced  iron,  saccharated 
solution  of  iron,  and  albuminate  of  iron  produced  no  ill  effects  either 
local  or  through  systemic  action. 

The  acid  vomitus  of  pregnancy  and  seasickness  have  an  analogous 
effect.  It  is  not  likely,  however,  that  during  a  transatlantic  voyage 
large  cavities  can  develop.  The  probable. explanation  of  the  presence 
of  such  cavities  directly  after  the  voyage  is  that  they  existed  before 
the  voyage  was  begun.  Cavities  are  frequently  left  or  overlooked. 
(See  Prophylaxis  of  Caries.)  Since  the  advent  of  medication  by 
lactic  acid  preparations  and  those  containing  lactic  acid  bacilli,  such 
as  sour  milk,  analogous  effects  have  been  observed,  and  therefore  the 
mouth  should  be  washed  out  with  alkaline  antiseptics  after  such 
remedies  are  taken.^ 

Miller  found  that  the  saliva  has  no  antiseptic  quality  as  a  whole 
and  contains  no  antiseptic  substance,  and  though  he  found  the  saliva 
of  immunes  to  develop  a  little  less  acid  than  that  of  highly  susceptible 
individuals,  the  difference  was  not  constant  and  not  sufficient  to 
account  for  the  marked  difference  in  susceptibility.  Miller  found  that 
carbohydrate  foodstuffs  mixed  with  an  alkaline  saliva  became  even 
more  acid  than  when  the  reaction  of  the  saliva  was  intensely  acid 
and  the  chance  for  caries  was  about  the  same  with  either  reaction 
at  the  start.  Goadby^  calls  attention  to  the  demonstration  of  Savarelli 
that  saliva  is  germicidal  for  small  quantities  of  bacteria  but  loses 
its  property  wdth  large  quantities.  This  may  have  some  bearing 
on  caries. 

Under  conditions  of  oral  irritation,  such  as  catarrhal  stomatitis, 
or  even  the  presence  of  many  cavities  of  decay,  a  stringy,  mucinous 
condition  of  the  saliva  may  result.  This  may  be  due  to  a  partial 
coagulation  of  the  mucin  by  the  acid  present  in  the  mouth,  and  the 
coagulum  may  entangle  food  masses  and  cause  their  adherence  to 
the  teeth. 

Lack  of  Saliva  of  Alkaline  Potential. — Pickerill,^  in  exhaustive 
experiments,  shows  that  a  continuous  flow  of  saliva  may  be  refiexly 

1  Dental  Cosmos,  January,   1913,  p.  39. 

2  Therapeutische  Monatshefte,  1908.  ^  Vanel,  Dental  Cosmos,  1904,  p.  694. 
*  Mycology  of  the  Mouth. 

5  The  Prevention  of  Caries  and  Oral  Sepsis,  2d  Ed. 


PREDISPOSING  CAUSES  355 

excited  by  foodstuffs  having  taste  and  flavor,  and  especially  by 
organic  acids  of  fruit,  and  argues  that  such  alkaline  saliva  by  flowing 
over  teeth  neutralizes  any  acid  formed  by  fermentation.  Per  contra, 
its  absence  may  be  a  cause  of  caries.  The  argument  looks  rational, 
but  Pickerill  has  not  given  any  experiments  upon  susceptible  in- 
dividuals to  prove  his  case. 

Very  dry  mouths  have  a  viscid,  tenacious  saliva,  and  usually 
cervical  caries  is  present.  Some  individuals  are  greatly  incon- 
venienced and  may  have  to  frequently  moisten  the  mouth  to 
obtain  comfort. 

The  contention  of  Lohmann  that  the  carbohydrate  element  in 
mucin  was  the  cause  of  caries.  Miller  examined  experimentally  and 
found  it  untenable,  but  that  the  explanation  here  given  of  its  entan- 
gling action  is  the  probable  one.  He  states  that  very  small  amounts 
of  lactic  acid  precipitate  the  mucin  and  thus  enable  the  bacteria  to 
become  fixed  to  the  teeth  as  plaques. 

Miller  has  noted  that  some  immunes  have  had  exceedingly  ropy 
saliva  which  could  be  drawn  out  into  long  threads,  while  much 
caries  was  noted  in  the  mouths  of  some  almost  absolutely  free  from 
mucus. 

Miller  could  find  no  antiseptic  quality  in  the  saliva,  nor  any  prin- 
ciple corresponding  to  alexin,  and  found  that  bacteria  developed  in 
the  saliva  of  immunes  almost  as  readily  as  in  that  of  those  susceptible 
to  caries. 

He  also  pointed  out  that  the  mucus  may  readily  undergo  putre- 
factive fermentation  with  alkaline  reaction,  and,  again,  the  carbo- 
hydrates entangled  in  it  will  ferment  with  acid  reaction,  causing  any 
caries  which  might  be  attributable  to  mucin  fermentation.  Gies^ 
has  shown  that  salivary  mucin  forms  viscid  films  on  the  teeth, 
which  tend  to  thicken  by  accretion  and  in  which  millions  of 
bacteria  multiply,  particularly  at  night,  when  the  secretions  are 
strongest. 

It  is  possible  that  the  secretion  from  the  gum  may  in  some  cases 
be  acid  and  favor  the  production  of  caries  by  decalcifying  the  enamel 
about  the  cervix  (Fig.  321). 

Cook  has  shown  that  glycogenic  infiltration  of  the  oral  mucous 
membrane  may  be  produced  by  the  use  of  irritant  or  astringent 
washes,  which  may  possibly  permit  a  change  of  this  substance  by 
bacteria  into  acid  about  the  necks  of  teeth,  accounting  for  a  certain 
form  of  cervical  decay  long  thought  to  be  due  to  an  acid  mucus. 
(See  Glycogenic  Infiltration.) 

1  Journal  of  the  Allied  Societies,  June,  1912. 


356  DENTAL  CARIES 

Systemic  Predisposing  Causes. — Some  individuals  seem  to 
suffer  much  from  caries;  others  in  less  degree.  In  either  case,  periods 
of  immunity  or  comparative  immunity  may  be  established,  and  may 
be  again  followed  by  a  period  of  susceptibility  and  a  succeeding 
immunity. 

These  facts  point  to  the  conclusion  that  a  period  of  caries  is  due 
either  (1)  to  a  temporary  lack  of  oral  hygiene  with  a  corresponding 
intensity  in  oral  fermentation — i.  e.,  the  exciting  cause  is  active — or 
(2)  that  it  is  due  to  some  systemic  condition  which  changes  the  con- 
stitution of  the  oral  fluids,  permitting  the  formation  of  the  microbic 
plaques  upon  the  teeth,  or  (3)  increases  the  fermentation  by  supplying 
some  element  nutritive  to  bacteria  or  (4)  depriving  it  of  some  element 
inhibiting  the  growth  of  bacteria. 

Black  has  shown  that  caries  fungi  are  always  present  in  the  mouth, 
but  do  not  always  form  the  plaques.  Cases  also  exist  in  which  caries 
has  begun  during  some  period  of  susceptibility  and  a  number  of  new 
cavities  have  been  started.  Later  a  period  of  immunity  has  followed 
and  the  cavities  have  not  progressed. 

So  far  as  classed,  systemic  conditions  influencing  susceptibility 
and  immunity  may  be  placed  under  the  four  headings:  Heredity, 
Prenatal  and  Postnatal  Influences,  Age,  and  Bodily  Condition. 

Heredity. — Black^  records  observations  on  certain  families  as 
showing  a  tendency  to  caries  of  certain  teeth  at  a  given  age,  or  in 
certain  positions  upon  the  teeth,  e.  g.,  occlusal  pits.  In  certain  cases 
the  hereditary  tendency  persists.  This  tendency  must  be  due  either 
to  an  inherited  cell  physiology,  or  diet  tendency  influencing  the  oral 
fluid,  or  to  transmitted  faults  of  form  or,  possibly,  of  structure  of 
the  teeth. 

Prenatal  and  Postnatal  Influences. — It  is  quite  probable  that 
the  systemic  condition  of  the  mother  during  gestation  may  pro- 
foundly modify  the  anatomicophysiological  condition  of  the  body 
cells  of  the  child;  nutritional  processes  may  suffer  and  the  postnatal 
tooth  development  proceed  irregularly,  structure  being  affected; 
moreover,  the  altered  biochemical  function  of  the  cells  may  stand 
in  close  relation  to  the  constitution  of  the  oral  fluids,  and  these  in 
turn  may  favor  the  development  of  caries  fungi.  If,  therefore,  the 
mother  is  not  properly  nourished,  the  teeth  may  not  be  well  con- 
structed, especially  if  lime  be  lacking  in  her  food.  The  same  line  of 
argument  may  be  applied  to  bottle  feeding  of  recently  born  infants, 
or  to  other  conditions  profoundly  affecting  general  nutrition.  In 
this  connection,  the  absence  of  the  influence  of  the  internal  secretion 

1  Dental  Cosmos,  1904. 


PREDISPOSING  CAUSES  357 

which  should  be  transmitted  from  mother  to  child  by  way  of  the 
milk,  may  in  the  future  be  shown  to  have  a  bearing  upon  cell  develop- 
ment and  consequently  upon  the  product  (as  the  enamel). 

In  an  examination  of  school  children,  Th.  Frick^  (Zurich)  found  a 
much  greater  percentage  of  decay  in  children  that  had  been  bottle- 
fed  at  between  three  and  six  months  of  age.  He  performed  an  experi- 
ment on  a  litter  of  six  dogs,  feeding  three  on  cows'  milk  and  bouillon; 
one  of  them  died,  and  the  others  had  poorly  developed  teeth.  The 
controls  were  normal. 

Forberg  and  Rose'^  have  shown  that  the  individuals  who  drink 
water  rich  in  calcium  salts  have  a  smaller  percentage  of  caries  than 
those  drinking  soft  waters.  Ferrier  has  observed  a  coincidence  of 
caries  and  the  drinking  of  boiled  water  which  had  been  deprived  of 
calcium  carbonate.  Whether  this  effect  is  due  to  a  better  develop- 
ment of  tooth  structure  or  is  a  post-developmental  effect  is  not  stated 
in  either  case.  The  point  brought  up  by  Head,^  who  has  shown 
the  apparent  rehardening  of  teeth  in  saliva  after  partial  decalcifica- 
tion by  a  weak  acid,  opens  up  the  question  here  as  to  whether  the  use 
of  calcareous  waters  after  tooth  eruption  can  increase  the  density  of 
enamel.  Enamel  can  be  dried,  why  then  not  infiltrated  by  calcareous 
solutions?  The  question  cannot  now  be  answered.  Another  view 
might  be  that  some  of  the  calcium  salts  in  drinking  water  come 
back  to  the  saliva  eventually,  and  if  abundant  may  neutralize  the 
acidity  in  plaques,  through  their  alkalinity,  by  combining  with  the 
acids  formed. 

Age. — That  the  age  has  an  influence  upon  caries  was  noted  by 
Flagg.  He  recorded  the  ages  from  five  to  eight,  twelve  to  twenty, 
thirty  to  thirty-five,  forty-five  to  fifty,  sixty  to  sixty-five  years,  and 
senility  as  periods  of  decay,  while  the  intervening  periods  were 
intervals  of  comparative  exemption. 

Black  has  noted  that  caries  is  a  disease  of  youth,  most  intense 
before  adult  age,  at  which  time  immunity  is  established,  provided  the 
teeth  have  been  well  and  promptly  filled  and  the  mouth  otherwise 
cared  for.  In  view  of  this  fact,  he  aims  at  establishing  this  immunity 
by  close  attention  to  the  teeth  during  youth. 

He  records  fluctuations  in  susceptibility  not  unlike  those  recorded 
by  Flagg,  and  also  points  out  that  some  persons  pass  through  the 
ordinary  periods  of  susceptibility  and  first  develop  caries  in  middle 
age.  In  old  age,  general  recession  of  the  gum  is  common,  and  in  the 
conditions  of  debility  associated  with  old  age,  much  caries  of  cemen- 
tum  occurs.  The  patients  are  often  either  unwilling  or  unable  to 
keep  the  cementum  cleansed. 

1  Dental  Cosmos,  1901.  2  Ibid.,  1899.  3  gee  p.  315. 


358  DENTAL  CARIES 

Repeated  examinations  of  the  mouths  of  school-children  show  a 
deplorable  amount  of  caries  which  may,  perhaps,  be  attributable  to 
several  causes,  such  as  the  induction  of  a  lessened  systemic  resistance 
due  to  confinement,  study,  etc.,  and  also  to  the  inhalation  of  vitiated 
air,  which  presumably  also  contains  acid-producing  bacteria.  More- 
over, bacteria  of  caries  may  be  directly  transmitted  by  kissing, 
common  use  of  drinking  cups,  pencils,  etc. 

Michaels,^  of  Paris,  has  observed  that  "the  saliva  of  adolescence 
contains  a  dextrinic  principle  (glycogen)  susceptible  of  fermentation 
under  the  influence  of  ptyalin  in  the  presence  of  earthy  salts.  Lactic 
acid  is  formed."    (See  p.  98.) 

Bodily  Condition. — It  is  a  matter  of  observation  that  such  con- 
ditions as  pregnancy,  typhoid  fever,  anemia,  leukemia,  diabetes, 
dyspepsia,  nervous  exhaustion,  and  debility  are  frequently  accom- 
panied by  or  followed  by  a  development  of  cavities  of  decay,  but 
whether  the  diseases  themselves  or  a  coincident  lack  of  oral  hygiene 
act  to  permit  the  formation  of  the  microbic  plaques  has  not  clearly 
been  made  out.  If  oral  and  dental  prophylaxis  be  practised  during 
typhoid  fever  and  convalescence  therefrom,  the  production  of 
cavities  is  much  limited,  but  this  does  not  prove  anything.^  The  same 
is  true  of  pregnancy,  which  introduces  an  exciting  cause  (the  vom- 
itus),  and  of  glycosuria,  which  may  introduce  glucose,  or  a  ferment- 
able substance  as  claimed  by  Michael,^  according  to  whom  it  takes 
a  red  coloration  with  Nessler's  reagent,  which  passes  into  a  grayish 
blue.  Black  contends  that  periods  of  susceptibility  are  noted  both 
in  apparent  good  and  ill  health.  That  apparent  health  may  really 
not  be  true  health  is  a  matter  that  must  be  considered. 

This  bodily  condition  is  seemingly  the  key  to  any  change  which 
can  occur  in  saliva,  or  mucus,  or  oral  phagocytosis,  to  one  of  which 
must  be  attributed  any  possible  systemic  effect  upon  caries  bacteria, 
which  can  aid  or  inhibit  their  growth  or  localization.  It  matters  very 
little  whether  the  bodily  condition  is  due  to  heredity  as  a  general 
modification  of  cell  physiology,  to  age,  or  some  period  of  stress,  as 
the  "change"  of  the  teeth,  puberty,  growth  during  adolescence, 
diet,  business  or  family  anxieties,  the  degenerative  tendencies  of 
advancing  age,  or  to  some  more  acute  systemic  condition,  as  typhoid 
fever,  diabetes,  etc.,  except  in  so  far  as  these  conditions  may  intro- 
duce into  the  oral  fluid  a  substance  which  may  act  either  (1)  as  a 

1  Sialosemeiology.     See  Dental  Cosmos,  1900. 

2  A  caries  susceptible  was  treated  before  pregnancy  and  during  lactation  for  many 
cavities.  The  value  of  prophylaxis  was  finally  so  impressed  upon  her  that  she  practised 
it  properly.  Since  then  she  has  had  typhoid  fever,  but  no  increase  in  caries;  which 
amounts  Only  to  about  one  small  cavity  a  year. 

^  Quoted  by  Kirk,  see  Dental  Cosmos,  January,  1914,  p.  5. 


PREDISPOSING  CAUSES  359 

direct  decalcifying  agent  (an  acid)  or  (2)  as  an  indirect  decalcifying 
agent,  by  furnishing  a  food  material  for  the  bacteria  from  which  they 
may  manufacture  acid  (a  carbohydrate),  or  (3)  furnish  a  substance 
in  the  saliva  which  may  glue  the  germs  to  the  teeth,  or  (4)  take  from 
the  saliva  some  substance  which  normally  inhibits  plaque  formation. 

It  was  shown  under  the  caption  of  Erosion,  that  a  very  weak  acid 
may  decalcify  more  rapidly  than  a  stronger  solution,  and  it  has 
been  noted  that  in  systemic  conditions  inducing  general  acidosis 
(as  chronic  nephritis  or  diabetes)  there  is  a  tendency  to  deep  decalci- 
fication of  cervices  of  teeth,  beginning  particularly  upon  the  cemen- 
tum.  While  by  no  means  proved  not  due  largely  to  fermentation  of 
carbohydrate  food  by  bacterial  plaques,  as  a  result  of  defective 
hygiene,  there  is,  nevertheless,  a  strong  suspicion  that  the  acidosis 
expressed  as  acidity  of  saliva  has  produced  the  decalcification.  There 
is  also  a  probable  reduction  in  the  amount  of  normal  sodium  phos- 
phates as  the  result  of  the  general  acidosis,  and  this  also  found  in 
the  saliva  reduces  the  controlling  quality,  which  Head  has  shown 
to  exist  when  a  certain  percentage  of  basic  sodium  phosphate  is 
present  in  solutions  having  an  acid  reaction.  (See  p.  315.)  On 
the  other  hand,  in  such  a  condition  as  diabetes  there  is  not  only  a 
general  acidosis,  but  also  the  possible  transudation  of  a  glycogenic 
principle  into  the  saliva,  which  can  undergo  acid  fermentation  by 
oral  bacteria. 

Michaels^  states  that  the  constitution  of  the  saliva  changes  with 
the  establishment  of  various  diatheses,  and  that  a  physiological 
saliva  with  the  biochemical  principles  in  a  state  of  equilibrium  is 
probably  very  rare.  He  states  that  the  most  active  dental  caries  is 
found  in  the  mouths  of  hypo-acid  individuals,  in  whom  saline  chlorids 
predominate  over  the  acid  elements  of  metabolic  waste,  reducing  the 
acidity  of  body  fluids  below  normal,  and  inducing  a  lessened  resist- 
ance to  development  of  infective  causes,  and  that  caries  is  least  active 
in  the  hyperacid  individuals,  in  whom  sulphocyanid  of  potassium  is 
more  abundant  in  the  saliva.  He  has  also  claimed  to  have  found 
glycogen  in  the  saliva  of  adolescents.    (See  pp.  98  and  358.) 

Kirk^  claims  that  in  the  caries  susceptible,  the  saliva  is  alkaline  to 
litmus,  though  it  may  be  acid  to  other  reagents  (may  be  ampho- 
teric).' That  the  alkalinity  keeps  the  mucinous  elements  in  solution, 
and  at  the  same  time  a  substance  analogous  to  glycogen  and  fer- 
mentable by  caries  bacteria  is  transuded  by  the  salivary  glands, 
which  furnishes  the  bacteria  their  pabulum  after  their  fixation  in 
plaques  upon  the  teeth.    He  regards  this  glycogenic  principle  in  the 

1  Dental  Cosmos,  December,  1900. 

2  Items  of  Interest,  July,  1902,  p.  546. 


360  DENTAL  CARIES 

saliva  as  due  to  carbohydrate  diet  in  excess  of  the  body's  needs 
and  its  capability  of  storage  as  fat;  that  it  enters  the  blood  after 
the  glycogenic  function  of  the  liver  has  been  exerted  and  is  excreted 
in  the  saliva.  He  regards  the  variations  in  susceptibility  as  due  to 
variations  in  carbohydrate  diet. 

In  a  recent  article,'  the  possible  influence  of  the  hypophysis 
cerebri  upon  the  presence  of  an  excess  of  sugar  in  the  blood  and  of 
this  as  a  possible  explanation  of  caries  susceptibility,  is  treated  of 
by  Kirk,  who,  however,  disclaims  any  definite  finality  at  present. 

Pickerill  argues  that  as  glycogen  is  rapidly  converted  into  maltose 
and  iso-maltose  by  ptyalin,  glycogen  and  ptyalin  should  be  chemi- 
cally incompatible.  He  states  that  in  his  examination  of  the  saliva 
of  diabetics  and  those  suffering  from  other  disease,  no  sign  of  glucose 
has  been  present.  The  question  therefore  calls  for  investigation 
of  saliva  from  the  glands  direct,  to  avoid  mouth  glucose. 

Gies,2  conducting  elaborate  experiments  concerning  the  inhibitory 
effect  of  potassium  sulphocyanate  upon  plaque  formation,  concludes 
that  it  is  an  excretion  having  no  determined  bearing  upon  caries. 
Both  he  and  Howe'^  found  experimentally  that  it  did  not  inhibit 
bacterial  growth  in  cultures.  Howe  considers  it  increases  the  growth. 
Pickerill'*  seems  to  have  found  a  different  conclusion.  The  Com- 
mittee on  Scientific  Research  of  the  New  York  State  Dental  Society 
furnish  the  following  tests  for  it : 

Take  2  c.c.  of  saliva,  to  which  add  2  c.c.  of  distilled  water,  and 
shake  thoroughly  together.  Add  5  drops  of  iron  perchlorid,  and 
shake  again. 

The  presence  of  sulphocyanate  naturally  in  the  saliva  is  determined 
by  the  color. 

A  straw  color  indicates  little  or  none.  A  brick  color  indicates  a 
sufficiency.    A  wine  color  indicates  abundance. 

The  Committee  on  Scientific  Research,  of  the  National  Dental 
Association,^  have  devised  a  colorimetric  scale  which  consists  of  two 
tubes.  In  tube  A,  1  c.c.  of  saliva  is  placed.  In  tube  B,  1  c.c.  of  a  1  to 
2000  solution  of  sulphocyanate  of  ammonia.  To  each,  add  2  drops 
of  a  5  per  cent,  ferric  chlorid  solution  from  the  same  pipette.  Add 
distilled  water;  to  be  in  definite  quantities  until  the  color  matches 
that  of  the  saliva.  Calculation  of  the  dilution  of  the  standard 
solution  will  give  the  amount  of  sulphocyanate  in  the  saliva.  The 
observations  are  introduced,  that  others  may  continue  the  line  of 
thought. 

1  Dental  Cosmos,  January,  1914.  2  ibid.,  1913. 

3  The  Journal  of  The  Allied  Societies,  June,  1912. 
■•  The  Prevention  of  Dental  Caries  and  Oral  Sepsis. 
6  Dental  Cosmos,  1908,  p.  1365.. 


PREDISPOSING  CAUSES  361 

The  use  of  potassium  or  sodium  sulphocyanate  internally  in  | 
to  1  grain  doses,  in  tablet  form,  has  been  recommended  as  a  prophy- 
lactic, but  while  some  claim  value  it  is  quite  likely  that  other  means, 
such  as  oral  prophylaxis  conjoined  with  it,  have  had  much  to  do  with 
lessened  caries  and  hypersensitivity  of  dentin,  as  claimed. 

Potassium  sulphocyanate  is  described  as  a  nerve  tonic,  safe  in  even 
10  grain  doses.  It  must  not  be  confused  with  potassium  cyanate,  which 
is  a  virulent  poison. 

Kirk  has  succeeded  in  altering  viscid  saliva  to  a  more  limpid  condi- 
tion, by  reducing  the  ratio  of  carbohydrate  to  proteid  diet,  first  cutting 
out  carbohydrates  almost  altogether,  then  adding  them  gradually  to 
the  diet.  He  cites  observations  upon  asylum  children  kept  upon 
well-balanced  rations,  as  having  large  numbers  of  arrested  caries.^ 
(See  p.  359.) 

Black^  believes  that  the  condition  of  the  system  alters  the  oral 
fluid,  so  as  to  permit  the  bacteria  in  it  to  produce  a  gelatinoid  material 
as  a  by-product,  in  one  case  and  not  to  produce  it  in  another,  and 
that  when  produced,  plaques  adhere  to  the  teeth  in  sheltered  spots, 
while  when  not  produced  no  plaques  adhere,  though  a  general  acidity 
of  the  oral  fluids  may  be  produced. 

Miller,^  some  years  ago,  pointed  out  that  filthy  mouths  often  do 
not  contain  carious  teeth.  He  offered  the  rational  explanation  that 
the  unchanged  adhering  collections,  once  their  acid-producing  capa- 
city is  destroyed,  can  even  act  as  a  protection  in  so  far  as  caries  is 
concerned.  In  experiments  on  artificial  production  of  caries,  Miller 
found  that  the  pabulum  of  the  bacteria  needed  constant  change, 
otherwise  putrefaction  resulted  and  decay  ceased.  The  fact  that 
fairly  cared-for  mouths  often  contain  carious  teeth  is  rather  an 
argument  in  favor  of  the  local  etiology  of  caries,  as  teeth  unbrushed 
after  a  meal,  or,  rather,  not  thoroughly  cleansed,  as  is  the  rule  in  a 
vast  majority  of  mouths,  contain  every  necessary  factor  of  caries, 
including  a  renewal  of  fresh  carbohydrate  food  for  the  bacteria. 
As  prophylaxis  becomes  more  accurate,  mouths  usually  pass  into 
a  condition  suggesting  a  condition  of  immunity.  It  would  seem, 
therefore,  that  unless  some  other  factor  of  prophylaxis  can  be  intro- 
duced, the  mouth  should  either  be  thoroughly  cleansed  or  not  at  all, 
so  far  as  caries  is  concerned. 

The  whole  subject  of  susceptibility  and  immunity  to  caries  is  yet 
obscure  and  requires  accurate  experimental  study. 

1  Dental  Brief,  1907. 

2  Dental  Digest,  1907. 

^  Lecture  at  the  University  of  Pennsylvania. 


CHAPTER  XII. 

DENTAL  CARIES:  PATHOLOGY,  MORBID  ANATOMY, 
AND  CLINICAL  HISTORY. 

PATHOLOGY   AND   MORBID   ANATOMY. 

It  is  a  fact  of  common  observation  that  caries  begins  only  at 
spots  protected  from  friction  or  uncleansed.  These  are  in  order  of 
frequency:  (1)  Pits,  grooves,  and  fissures  in  the  enamel;  (2)  approxi- 
mal  surfaces  just  above  the  contact  point;  (3)  smooth  surfaces  which 


Fig.  322 


Fig.  323 


Fig.  324 


Fig.  325 


Fig.  326 


Fig.  333 


Fig.  327 


Fig.  328 


Fig.  331 


Fig.  335 


from  any  cause  are  habitually  unclean;  (4)  necks  of  the  teeth  at  or 
near  the  junction  of  the  cementum  and  enamel  (Black)  (Figs.  322 
to  335). 

In  these  situations  Williams  has  demonstrated  the  fact  that  the 
oral   bacteria,   protected   from   friction,   attach   themselves   to   the 
(362) 


PATHOLOGY  AND  MORBID  ANATOMY 


363 


enamel,  forming  microbic  plaques  which  are  sufficiently  adherent 
to  permit  their  retention  during  the  grinding  of  the  specimen  for 
microscopic  examination.  (See  Figs.  336,  337,  and  338.)  Carbo- 
hydrate food  debris  lodges  at  the  points  at  which  retention  is  favored, 
and  either  ferments  directly  against  the  enamel,  or  through  the 
medium  of  the  microbic  plaque. 

The  bacteria  in  the  plaque  require  food  and  obtain  it  from  the 
carbohydrate  and  albuminous  materials  which  come  in  contact  with 
them.     From  the  carbohydrates  lactic  acid  is  produced  as  a  waste 

Fig.  336 


Section  of  normal  human  enamel,  showing  thick,  felt-like  mass  of  microorganisms 
slightly  raised  from  the  surface  of  the  tissue,  by  pressure  of  the  cover-glass  in  mounting. 
X  250.     (Williams.) 

product.  (See  Chapter  XI.)  Williams  states  that  it  is  "highly  im- 
probable that  the  enamel  is  affected,  except  in  rare  and  special 
instances  by  any  other  acid  than  that  which  is  being  excreted  by  the 
bacteria  at  the  very  point  at  which  they  are  attached  to  the  enamel." 

This  thick  mass  of  fungi  also  prevents  the  excreted  acid  from 
being  washed  away,  so  that  it  exerts  its  full  chemical  power  upon 
calcific  tissue. 

The  lactic   acid   produced  attacks  the  inorganic  matter  of  the 


364 


DENTAL  CARIES 


enamel,  following  first  the  interprismatic  cement  substance  between 
the  prisms,  later  dissolving  the  transverse  cement  substance  between 
the  globules.  The  effect  is  to  produce  an  irregular,  roughened  sur- 
face of  the  enamel  and  to  bring  into  view  the  structure  of  the  rods 
(Figs.  337  and  343). 

Fig.  337 


Microorganisms  of  caries  attached  to  enamel  on  approximal  surface  of  tooth. 

(WiUiams.) 


The  gradual  loss  of  cement  substance  unbinds  the  enamel  globules, 
which  are  in  turn  dissolved  and  washed  away,  leaving  a  depression 
or  cavity. 

In  the  process  of  enamel  dissolution,  the  bacteria  may  enter  the 
crevices  formed  by  solution  of  the  interprismatic  cement  substance, 
and  by  repetition  of  the  process  gain  access  to  the  dentin  (Fig.  346). 

The  form  of  the  enamel  may  be  retained  until  and  even  after 
decalcification  has  reached  the  dentin.     Clinically,  this  is  seen  as  an 


PATHOLOGY  AND  MORBID  ANATOMY  365 

Fig.  338 


Superficial  approximal  caries  of  enamel  with  films;  also  shows  sHght  approximal 

abrasion.     (Miller.) 


Fig.  339 


Budding  of  spores  on  the  stems  of  Leptothrix  racemosa.     (Williams.) 


366  DENTAL  CARIES 

opaque  white  or  discolored  spot,  resisting  the  instrument  until  some 
force  is  used,  when  it  rapidly  breaks  down  (Figs.  338  and  347). 

A  central  cavity,  or  several  minute  openings,  leading  to  or  almost 
to  the  dentin,  is  sometimes  seen  in  the  general  decalcified  area.  It 
signifies  the  loss  of  the  organic  matter  of  the  enamel,  by  unbinding  or 

Fig.  340 


m^SL 


Thick  growth  of  Leptothrix  racemosa  fructification  heads  from  approximal  surface  of 
tooth,  under  high  magnifying  power.     (Wilhams.) 


peptonizing  actions.  The  extraction  of  an  approximating  tooth 
permits  the  film  to  be  rubbed  off,  or  prevents  the  retention  of  carbo- 
hydrate media,  so  that  the  bacteria  cease  to  be  active,  and  this  spot 
may  remain  indefinitely  at  this  point — e.  g.,  the  disease  is  arrested. 
It  may  cease  spontaneously  to  develop  further,  owing  to  the  estab- 
lishment of  an  immunizing  sj^stemic  change,  even  though  the  teeth 


PATHOLOGY  AND  MORBID  ANATOMY 
Fig.  341 


367 


A  form  of  streptococcus  found  abundantly  in  mouths  where  very  rapid  decay  of  teeth 
is  in  progress.     X  750.     (Williams.) 

Fig.  342      - 


Scrapings  of  microorganisms  from  the  approximal  surface  of  a  decaying  tooth :  shows 
the  Leptothrix  buccalis  maxima  and  the  Bacillus  bucallis  maximus  of  Miller.  X  1500. 
(WiUiams.) 


368 


DENTAL  CARIES 


remain  in  approximation,  and  strict  prophylaxis  will  usually  arrest 
the  advance  of  the  process. 

It  is  also  noted  clinically  and  microscopically  that  the  decalcifica- 
tion is  deepest  at  a  spot  just  above  the  point  of  contact,  and  less 
deep  at  points  buccal  or  lingual,  occlusal  or  cervical,  to  this  spot, 
and  still  less  at  points  more  buccal  or  lingual — i.  e.,  it  shades  off  to 
zero  lingually,  buccally,  occlusally,  and  cervically  (Fig.  347).  The 
dentin  may  in  such  cases  be  deeply  affected.  Bacteria  growing  in 
the  spaces  from  which  the  interprismatic  cement  substance  has  dis- 
appeared, causes  detachment  of  masses  of  partially  decalcified  rods 
(Figs.  346  and  348). 

Fig.  .343 


Section  through  human  enamel,  showing  first  stages  of  caries,  i.  e.,  solution  of  inter- 
prismatic cement  substance.   To  be  compared  with  Fig.  177.   (Williams.) 

When  the  entire  thickness  of  the  enamel  is  penetrated  and  the 
dentin  attacked,  there  is  a  change  in  the  mode  of  progress  of  the 
decalcification,  which  proceeds  along  the  line  of  union  between  the 
enamel  and  dentin,  as  well  as  directly  into  the  dentin  (Fig.  347) ;  in 
this  way  the  enamel  is  attacked  from  its  dentinal  side  (backward 
caries)  (Fig.  345). 


PATHOLOGY  AND  MORBID  ANATOMY  369 

In  the  ultimate  breaking  down  of  the  enamel  the  rods  first  separate; 
the  outlines  of  the  several  globules  of  which  the  rods  are  composed  are 
brought  into  plain  view;  next,  the  calcified  plasmic  strings  noted  in 
enamel  formation  become  evident;  and  finally,  the  bead-like  masses 
upon  these  strings  are  left  as  the  ultimate  granular  detritus  of  the 
enamel. 

In  cases  of  rapid  enamel  dissolution,  Williams  found  streptococci 
almost  invariably  present;  and  suggests  tentatively  that  the  variety 
of  organism  may  be  the  factor  governing  the  rapidity  of  dissolution 
(Fig.  341).     (See  Miller,  p.  344.) 

Fig.  344 


Section  of  human  bicuspid,  showing  commencement  of  caries:  a  and  a',  appearances 
caused  in  enamel  and  dentin  by  the  acid  of  decay;  b  and  h-,  shreds  of  a  felt-like  mass 
of  bacteria  raised  from  the  surface  of  the  enamel;  c,  a  cavity.     X  12.     (Williams.) 

These  are  probably  the  Streptotoccus  brevis,  of  Goadby  (Micro- 
coccus nexifer,  of  Miller) . 

Williams  found  Streptococcus  pyogenes  albus  and  aureus  and 
Sarcinea  lutea  to  be  acid  producers. 

The  large  cocci  and  diplococci  shown  in  Fig.  349  were  always 
found  in  the  secondary  decay  of  enamel. 

"  In  the  direct  caries  of  enamel,  the  cavities  are  lined  with  leptothrix 
and  thread-like  forms." 
24 


370 


DENTAL  CARIES 


"The  Leptothrix  buccalis  maxima  and  the  Bacillus  biiccalis 
maximus,  of  Miller,  are  nearly  always  found,  the  latter  more  spar- 
ingly" (Fig.  342). 

Fig.  345 


Section  of  carious  tooth,  showing  appearances  of  decay  in  enamel  and  dentin  at  the 
line  of  union  of  these  tissues;  the  dark  spots  shown  in  the  enamel  and  dentin  are 
masses  of  microorganisms.      X  250.     (Williams.) 


Fig.  346 


Penetration  of  bacilli  between  enamel  prisms  after  solution  of  interprismatic  cement 

substance.     (Miller.) 


PATHOLOGY  AND  MORBID  ANATOMY 


371 


Some  of  these  bacteria  are  not  acid  producers,  and  it  may  be  that 
if  a  film  is  composed  entirely  of  these,  they  may  occupy  a  field  and 
really  protect  it  by  excluding  acid-forming  bacteria. 

"Beneath  the  felt-like  masses  of  thread  forms,  and  lying  in  contact 
with  the  decomposing  enamel  in  direct  decay,  and  also  in  deep  cracks 
and  fissures  in  secondary  decay,  there  is  invariably  found  a  short, 
thick  bacillus,  usually  constricted  in  the  centre."  (Williams,  also 
Goadby.) 

Fig.  347 


Decalcification  of  enamel  without  loss  of  form;  a,  film.      X  35.     (Miller.) 


Caries  of  Nasmyth's  Membrane.— Miller^  demonstrated  that  the 
enamel  cuticle  may  act  as  a  breeding  ground  for  many  forms  of 
bacteria^ which  occupy  it,  forming  a  matrix  which  may  retain  minute 
particles  of  food,  which  in  turn  aid  in  acceleration  of  the  progress 
of  decay  (Fig.  351). 

Caries  of  Dentin. — The  bacteria,  after  penetrating  the  substance 
of  the  enamel,  attack  the  dentin.  This  presents  a  different  anatomical 
and  chemical  structure  to  be  acted  upon.  Beneath  the  enamel,  the 
first  layer  of  dentin  is  of  a  composition  which  permits  the  bacteria 
to  rapidly  spread  laterally  along  this  zone.     They  also  enter  the 

1  Microorganisms  of  the  Human  Mouth,  1890,  and  Dental  Cosmos,  1900. 


372 


DENTAL  CARIES 


tubules  of  the  dentin,  and  penetrate  by  multiplication,  toward  the 
pulp.  A  wedge-shaped  area  of  decay  is  produced  (Figs.  347  and  353). 
In  all  cases  decalcification  precedes  these  invasions.  At  the 
periphery,  the  tubules  communicate  freely  by  their  lateral  branches 
(Fig.  352),  and  the  lateral  spreading  of  the  bacteria  by  multiplication 
is  readily  explained. 

Fig.  348 


Cover-glass  preparation  from  scrapings  of  white,  opaque,  decaying  enamel;  the 
cement  substance  between  the  rods  is  seen  to  be  dissolved  away,  and  the  crevices  thus 
formed  are  filled  with  round  and  oval  forms  of  micrococci  and  bacteria.  Stained  by 
the  Gram  method.     X  450.     (Williams.) 


It  is  seen  clinically  in  caries,  that  a  portion  of  the  dentin  is  abso- 
lutely destroyed  and  removed,  leaving  within  the  tooth  a  "  cavity  of 
decay,"  bounded  by  dentin  and  enamel  undergoing  disintegration; 
beneath  this  lies  dentin  less  affected,  and  beneath  this,  sound  dentin 
(Fig.  353).  |t These  phenomena  require  explanation. 

The  tubules  of  the  decalcified  dentin  become  packed  for  a  distance, 
with  bacteria  (Fig.  354).  These  act  upon  the  organic  matrix  of  the 
decalcified  tubule  walls.    The  internal  pressure  due  to  multiplication 


PATHOLOGY  AND  MORBID  ANATOMY 
Fig.  349 


37; 


Various  forms  of  ^  micrococci  and  bacteria  from  decaying  enamel.       Photographed  by- 
Mr.  Andrew  Pringle  from  Williams'  cover-glass  preparation.     X  1000.  (Williams.) 

Fig.  350 


Cover-glass   preparations   of   scrapings   from    decay   of   enamel;  shows   Leptothrix 
bucalhs  maxima  and  Bacillus  bucallis  maximus,  of  Miller.    Stained  by  Gram  method 
X  830.     (Williams.) 


374 


DENTAL  CARIES 


distends  them  so  that  the  lumen  is  enlarged.  At  the  same  time,  the 
bacteria  excrete  a  ferment  or  ferments  which  cause  the  wall  at  first 
to  thicken.    The  dilatation  and  thickening  together  cause  the  com- 


FiG.  351 


Enamel  cuticle  permeated  by  bacteria.     (1100  to  1.)     (Miller.) 
Fig.  352 


Carious  dentin,  stained  with  fuchsin  to  show  microorganisms.  The  section  shows 
the  condition  of  the  tubules  as  filled  with  microorganisms  along  the  junction  of  the 
dentin  with  the  enamel  at  a.  The  tubules  are  very  much  enlarged.  (1/10  immersion 
objective.)     (Black.) 

pression  of  the  decalcified  intertubular  substance,  and  the  tubules 
assume  an  hexagonal  shape  owing  to  the  mutual  pressure  (Fig.  355) . 
The  phenomenon  is  not  a  vital  one,  as  it  occurs  in  artificial  caries. 
(Miller.) 


PATHOLOGY  AND  MORBID  ANATOMY 


375 


The  bacterial  ferment  possesses  a  digestive  or  peptonizing  power, 
analogous  to  trypsin,  and  begins  to  liquefy  the  inner  surface  of  the 
tubule  wall.     As  it  does  so,  the  lumen  is  further  increased  and  the 


Fig.  353 


Longitudinal  ground-section  through  the  crown  of  an  inferior  molar  of  a  negro: 
E,  enamel;  D,  dentin;  C,  cement;  p,  pulp  chamber;  a,  large  decay,  from  the  occlusal 
surface;  h,  small  decay,  from  the  mesial  surface;  c  s,  cone  of  septic  invasion  and 
discoloration;  e,  partially  decalcified  and  discolored  enamel  around  the  carious  cavity; 
2,  dark  cones;  z' ,  clearer  cones;  z'p,  oldest  cones  where  putrefaction  of  the  tooth  cartilage 
begins;  c,  outer  transparent  zone,  or  zone  of  Tomes;  s  d,  secondary  dentin,  caused  by 
irritation;  s'  d' ,  secondary  dentin  deposited  by  normal  physiological  process,  recession 
of  the  pulp.  This  figure  is  drawn  from  a  ground  and  polished  section  mounted  in 
Canada  balsam.     (Gysi.) 


376 


DENTAL  CARIES 


bacteria  fill  the  acquired  space.     Taking  up  carbohydrates,  lactic 
acid  is  produced,  which  combines  with  the  calcium  salts  of  deeper 

tubules  and  intertubular   substance  and 
^^°'  ^^^  prepares  a  path  of  decalcified  tissue  for 

bacterial  advance  (Fig.  356).  This  de- 
calcified tissue,  to  all  intents  and  pur- 
poses, becomes  a  culture  medium. 

Fig.  355 


Carious  dentin,   showing    in^ 

invaded  tubules  and  uninvaded  Cross-section    of    decayed    dentin:  the    tubules 

but      decalcified      intertubular  through    reciprocal    pressure    have    assumed    the 

substance.    (Miller.)  shape  of  five-  and  six-sided  prisms.     (Miller.) 

This  combination  of  the  acid  with  the  calcium  salts  disposes  of 
or  neutralizes  the  acid,  which,  if  accumulated  to  the  strength  of 

Fig.  356 


'^'^ 


Section  of  decalcified  dentin  partly  invaded  by  bacteria:  a,  uninvaded  zone.     (Miller.) 


2  per  cent.,  would  cause  the  destruction  of  the  bacteria,  by  their 
waste  products.  (Miller.)  Calcium  lactophosphate,  calcium  lactate, 
and  magnesium  lactophosphate  are  produced.    This  point  has  been 


PATHOLOGY  AND  MORBID  ANATOMY 


377 


illuminated  by  Pickerill/  who  placed  teeth  in  a  definite  quantity 
of  a  known  solution  of  lactic  acid.  This  at  first  decalcified  the  teeth 
rapidly,  but  after  thirty  days,  fresh  teeth  placed  in  the  solution  for 
twenty  days  were  barely  affected  thus  showing  an  exhaustion  or 
neutralization  of  the  acid. 

Miller  experimentally  found  that  the  calcium  carbonate  does  so 
neutralize  the  acid  formed  by  formation  of  calcium  lactate,  but 


Fig.  357 


Fig.  358 


"   ^  tl 


/I 


Decayed  dentin  showing  a 
mixed  infection  with  cocci  and 
bacilli.       X    400.      (Miller.) 


Liquefaction  foci.     (Miller.) 


the  calcium  phosphate  does  not,  as  it 
develops  calcium  lactophosphate,  setting 
free  phosphoric  acid,  which  maintains  the 
relative  acidity.  Experimentally,  the  addi- 
tion of  calcium  phosphate  to  a  solution 
of  lactic  acid  did  not  reduce  the  decalci- 
fication in  pieces  of  dentin  placed  in  it, 

for  the  reason  named.  Howe^  determined  by  experiments  'that  a 
slight  increase  in  phosphate  produces  great  activity  of  bacteria  in 
a  starch  or  sugar  solution,  with  large  and  rapid  formation  of  acid.' 
That  this  is  true  also  of  the  alcoholic  fermentation  (yeast)  and  in 
milk.  The  presence  of  chlorids  he  found  to  restrain  fermentation. 
The  bacterial  ferments  continue  to  digest  the  wall  of  the  tubule, 
and  a  time  arrives  when  they  have  penetrated  its  substance.  The 
intertubular  substance  is  then  removed  in  like  manner.    The  same 


1  The  Prevention  of  Dental  Caries  and  Oral  Sepsis,    2d  Ed.,  p.  22. 

2  The  Journal  of  The  Allied  Societies,  June,  1912. 


378  DENTAL  CARIES 

process  occurring  in  adjoining  tubules  as  well,  the  entire  dentinal 
substance  in  the  particular  area  at  the  cavity  surface  is  destroyed — 
i.  e.,  liquefied  and  washed  away  (Fig.  353,  a).     A  cavity  results. 

Occurring  at  a  point  beneath  the  general  cavity  surface,  the 
bacteria  in  several  adjoining  tubules  destroy  their  walls  and  the 
intervening  intertubular  substance,  forming  what  Miller  has  called  a 
"liquefaction  focus"  (pi.  foci)  (Fig.  357).  This  action  proceeds  until 
the  enamel  is  undermined  and  the  pulp  is  exposed.  A  decalcified 
area  always  exists  in  advance  of  the  tubule  invasion,  sometimes  large 
masses  being  found,  though  it  lessens  in  quantity  as  the  pulp  is 
approached.  As  the  enamel  is  undermined  by  the  carious  process, 
the  bacteria  and  their  acids  decalcify  its  inner  surface,  the  process 
proceeding  from  within  outward,  and  termed  "secondary  caries,"  or 
"backward  caries,"  of  enamel  (Fig.  345). 

The  enamel  is  thus  weakened  and  at  the  same  time  deprived  of 
dentinal  support,  and  breaks  down  under  stress  of  mastication. 

Any  interglobular  spaces  in  the  dentin  being  filled  with  transi- 
tional or  uncalcified  material  like  the  tubule  walls  are  rapidly  invaded 
by  the  bacteria  during  their  progress  along  the  tubules  (Fig.  359) . 

The  character  of  the  organisms  in  the  tubules  and  the  nature  of 
the  liquefaction  seem  to  depend  upon  the  particular  germs  present. 

Miller  has  sho'U'n  that  in  the  deeper  portions  of  tubules  micrococci 
appear  to  predominate  over  the  rod  forms,  which  are  also  present; 
although  one  tubule  may  be  filled  with  cocci  and  its  neighbor  with 
rod  forms  (Fig.  358).  It  is  only  in  the  more  superficial  layers  that 
the  thread  forms  are  found  in  numbers. 

Goadby^  has  done  much  interesting  work  in  this  direction,  and 
offers  the  following  classification  of  bacteria  found  in  decayed  dentin : 

Bacterla.  of  Dental  Caries. 
Acid-forming  Bacteria. 
Streptococcus  brevis 

B.  necrodentalis \  Deep  layers  of  carious  dentin 

Staphylococcus  albus 
Streptococcus  brevis     •   . 
Sarcina  lutea   .... 

Sarcina  aurantiaca      ....{„         c   •  i  i  c        ■         j     x- 

c       ■         1,      /TT       IN  }  buperficial  layers  of  carious  dentin. 

Sarcina  alba  (iiisenberg)        .      .       I 

Staphylococcus  albus       ...       I 

Staphylococcus  aureus     ...      J 

Bacteria  which  Liquefy  Dentin  {Decalcified.) 
None  isolated  as  yet        ....  Deep  layers  of  carious  dentin. 
B.  mesentericus  ruber 


B.  mesentericus  vulgatus 
B.  mesentericus  fuscus     . 

B.  fervus 

B.  gingivae  pyogenes 

B.  liquefaciens  fiuorescens  motilis 

B.  subtilis 

Proteus  Zenkeri 

B.  plexiformis 


■  Superficial  layers  of  carious  dentin. 


1  Mycologj^  of  the  Mouth,  and  Dental  Cosmos. 


PATHOLOGY  AND  MORBID  ANATOMY  379 

Goadby  states  that  his  experiments  show  that  the  bacteria  which 
dissolve  blood  serum  also  digest  decalcified  dentin,  while  those  which 
only  liquefy  gelatin  do  not  digest  decalcified  dentin. 

His  experiments  also  indicate  that  of  the  bacteria  found  in  the 
superficial  layers  of  carious  dentin  some  produce  digestive  enzymes, 
others  acid  fermentation,  and  others  have  both  functions. 

Choquet^  has  confirmed  the  observation  of  Miller,  Vignal,  Gallipe, 
and  Goadby  that  the  deeper  the  portions  of  dentin  examined,  the 
fewer  species  of  fungi  are  found  in  the  tubules,  and  explains  it  upon 
the  ground  that  the  anaerobic  or  facultative  aerobic  organisms  in  the 
outer  layers  advance  into  the  deeper  dentin,  because  they  are  better 
suited  to  the  conditions.  Kirk  advances  the  as  yet  unproven  idea 
that  these  bacteria  grow  toward  the  pulp,  because  that  is  the  direc- 
tion of  their  food  supply,  i.  e.,  the  juices  in  the  protoplasm  of  the  part. 
In  this  connection,  the  demonstration  of  Goadby  that  some  bacteria 
liquefy  decalcified  dentin  shows  that  this  substance  is  a  food  supply. 

Fig.  359 
^^/■^  //// 


Interglobular  spaces  filled  with  bacteria.  (Miller.) 

These  exact  findings  are  interesting  as  bearing  out  the  general 
demonstrations  of  Miller;  at  the  same  time,  Miller's  experiment 
showing  absolute  dissolution  by  a  single  bacterium  in  pure  culture  is 
to  be  recalled.     (See  page  342.) 

Choquet^  has  shown  that  dental  caries  may  proceed  under  fillings 
against  sound  dentin  by  the  following  experiment: 

Artificial  cavities  were  prepared  in  the  incisors  of  a  sheep.  In  these 
was  securely  sealed  with  cement,  a  small  particle  of  a  gelatin  culture 
of  caries  fungi,  applied  on  a  sterilized  platinum  cap.  Nine  months 
later  the  dentin  had  become  yellow,  slightly  decalcified,  and  the 
tubules  penetrated  by  bacteria.    This  softened  dentin  was  used  to 

1  Microbes  of  Dental  Caries,  Dental  Cosmos,  1900. 

2  Ibid. 


380  DENTAL  CARIES 

inoculate  a  portion  of  the  medium  originally  used,  and  the  species 
again  cultivated. 

Miller^  estimated  the  relative  loss  of  inorganic  and  organic  matter 
in  dentin  during  the  process  of  caries,  by  weighing  and  analyzing 
equal  volumes  of  carious  and  sound  dentin  from  the  same  teeth. 

The  carious  dentin  had  lost  about  seven-ninths  of  its  weight, 
which  was  due  to  the  loss  of  twelve-thirteenths  of  its  original  calcium 
salts  by  decalcification,  and  two-fifths  of  its  original  organic  matter 
by  liquefaction  of  its  substance. 

Tube  Casts. — In  the  zone  of  decalcification,  in  advance  of  bacterial 
invasion  of  the  tubes,  are  found  rod-shaped  bodies  or  shining  granules, 
first  described  by  J.  Tomes.  They  occur  in  both  natural  and  artificial 
caries,  hence  it  must  be  inferred  that  their  presence  is  not  the  result 
of  a  vital  process. 

The  rods  do  not  dissolve  in  organic  acids,  but  dilute  sulphuric 
acid  quickly  dissolves  them.     They  are  unaffected  by  alcohol  or 
chloroform,  a  proof  that  they  are  not  composed 
Fig.  360  of  fat.     Miller  regards  them  as  probably  calcic 

formations  against  the  tubule  wall  as  a  cast  of 
the  wall,  and  which  become  loosened  when  en- 
largement of  the  tubule  occurs.  They  have  a 
tubular  structure,  are  brittle,  and  may  contain 
a  central  thread-like  filament  which  may  possi- 
bly be  the  remains  of  a  dentinal  fibril.  Bac- 
teria may  surround  them,  but  do  not  enter 
them.  The  granules  are  probably  broken  rods.^ 
Tube  casts.  The  data  point   toward  a  probability   that  the 

rods  are  composed  of  calcium  lactate  and  cal- 
cium lactophosphate,  the  result  of  a  combination  of  lactic  acid  with 
the  calcium  salts  of  the  dentin.  The  resultant  salt  is  probably  de- 
posited as  a  tube  cast,  as  suggested  by  Miller. 

The  Transparent  Zone. — Around  the  zone  of  decalcified  uninfected 
dentin  appears  a  zone  of  dentin  more  transparent  than  the  surround- 
ing normal  dentin.  The  zone  extends  from  periphery  to  periphery 
around  the  cone  of  carious  dentin  (Fig.  353,  c).  The  tubules  in  this 
area  contain  granular  matter  not  seen  in  normal  dentin,  nor  in  the 
dentin  of  dead  teeth  in  the  same  situation.^ 

Tomes  and  Magitot  both  regarded  the  transparency  as  an  attempt 
made  by  nature  to  impede  the  progress  of  caries.  Walkhoff  regards 
it  as  due  to  a  sclerotic  action,  the  fibrillse  upon  stimulation  producing 
intercellular   substance    (tubule   wall),  at   their   own   expense   and 

1  Microorganisms  of  tiie  Human  Mouth. 

2  Miller.  ''  Ibid. 


PATHOLOGY  AND  MORBID  ANATOMY  381 

primarily  of  their  offshoots.  Black  once  regarded  it  as  the  earliest 
stage  of  decalcification,  but  has  discarded  this  idea.  Miller  advanced 
the  following  data.^ 

1.  Transparency  indicates  increased  homogeneity  as  opposed  to 
the  heterogeneity  of  normal  dentin — i.  e.,  the  coefficients  of  light 
refraction  are  brought  nearer  together. 

Fig.  361 


Section   from  a  lower  incisor  worn  on  a  plate,  extensive  decay  without  increase  of 
transparency.    X  15.     (Miller.) 

2.  It  occurs  in  living  dentin  only  and  is  not  found  in  natural  teeth 
mounted  on  plates  and  decayed  in  the  mouth,  nor  in  secondary  caries 
of  dentin  from  the  pulp  cavit}^  to  the  periphery,  and  is,  therefore,  a 
result  of  vital  action.  (Compare  Figs.  353  and  363  with  Figs.  361 
and  362.) 

3.  The  tubules  have  their  lumen  lessened  in  diameter  in  the  trans- 
parent areas,  an  agreement  with  the  position  of  Walkhoff. 

4.  Secondary  dentin  may  accompany  the  process  in  contiguity 
with  the  area;  moreover,  secondary  dentin  is  translucent.  It  indi- 
cates a  constructive  excitation  of  the  odontoblasts,  of  which  the 
dentinal  fibrils  are  prolongations  (Figs.  353,  Sd). 

1  Microorganisms  of  the  Human  Mouth. 


382 


DENTAL  CARIES 


5.  Chemical  analysis  proved  that  no  lime  salts  had  been  lost,  and 
it  was  pointed  out  that  a  gain  in  the  percentage  of  salts  was  unneces- 
sary, as  new  dentin  is  necessarily  composed  of  organic  as  well  as 
inorganic  matter,  wherefore  the  analysis  would  not  necessarily  vary 
from  that  of  normal  dentin. 

6.  It  is  found  in  connection  with  abrasion  of  human  teeth  in  which 
the  activity  of  acid  may  possibly  be  an  open  question,  and  it  also 
occurs  in  the  worn  teeth  of  dogs,  the  saliva  of  which  is  strongly 
alkaline. 

Miller  states  that  opacity  may  follow  or  be  associated  with  trans- 
parency.^ 

Fig.  362 


Secondary  caries  of  dentin,  advancing  from  pulp  chamber  and   therefore  occurring 
after  death  of  the  pulp.  Absence  of  transparency.    X  15.   (Miller.) 

The  natural  conclusion  is  that  the  transparency  is  a  form  of 
tubular  calcification,  and  that  it  impedes  the  progress  of  caries;  that 
it  does  not  succeed,  as  a  rule,  is  due  to  the  overwhelming  action  of 
the  bacteria. 

In  cavities  from  which  the  walls  are  broken  away,  freely  exposing 
the  carious  dentin  to  mastication,  the  carious  dentin  and  its  con- 
tained bacteria  may  be  removed  by  friction  (Fig.  367,  B). 


I  Dental  Cosmos,  April,  1903. 


PATHOLOGY  AND  MORBID  ANATOMY 


383 


In  the  transparent  area,  the  tubules  become  obUterated ;  a  poHshed, 
discolored  surface  results,  resembling  in  degree  an  abraded  surface. 
This  process  is  called  "  eburnation,"  and  is  really  tubular  calcifica- 
tion (which  see).  In  the  same  tooth  a  more  sheltered  border  of  this 
spot  may  be  undergoing  the  carious  process.  Miller  records  cases  of 
badly  decayed  teeth,  in  which  the  process  ceased  spontaneously  and 
the  dentin  became  hard  and  smooth. 

Pigmentation  in  Caries. — Pigmentation  occurs  in  caries  possibly 
from  extraneous  substances  entering  the  carious  area,  possibly  from 
the  substances  formed  during  putrefaction. 

The  slower  the  progress  of  the  decay,  the  greater  the  discoloration. 
The  colors  vary  from  light  yellow  to  reddish  brown,  dark  brown, 
and  black. 

Fig.  363 


Transparency  resulting  from  cracks  in  the  enamel  at  a  and  b.      X  20.     (Miller.) 


The  color  is,  as  a  rule,  darkest  upon  the  outside  of  the  carious 
dentin,  but  the  pigment  may  extend  through  large  masses  and  be 
found  staining  dentin  beneath  the  caries,  hard  enough  to  leave  in 
situ.    As  a  rule,  this  is  not  the  case. 

Black  suggests  the  possible  formation  of  sulphids.  Miller  has 
found  iron  almost  constantly  present  in  carious  dentin.  The  dis- 
coloration of  dentin  does  not  seem  to  be  necessarily  due  to  the 
carious  process,  as  it  may  be  seen  in  areas  of  abrasion.    In  a  specimen 


384  DENTAL  CARIES 

possessed  by  the  editor,  a  limited  cervical  caries  caused  a  growth  of 
secondary  dentin  and  an  area  of  tubular  calcification.  From  the 
pulpal  surface  of  the  secondary  dentin  to  the  area  of  caries,  extends 
a  sharply  defined  area  which  has  a  flesh-rose  color  (Fig.  364).  Many 
areas  of  secondary  dentin  due  to  abrasion  are  stained  a  dark  brown. 

Artificial  caries  produced  in  teeth  placed  in  a  mixture  of  bread 
and  saliva,  and  the  mixture  constantly  renewed,  was  white.  If  putre- 
faction was  allowed  to  occur,  discolorations  ensued  (Miller). 

The  discolorations  of  carious  dentin  may  be  due  to  the  action  of 
chromogenic  bacteria.  Miller  isolated  from  the  mouth,  an  organism 
which  he  named  Bacillus  fuscans,  and  "which,  cultivated  on  the 
surface  of  nutritive  agar-agar,  in  a  few  weeks  imparts  to  the  medium 
a  yellowish-brown  color,  which  gradually  darkens  and  extends 
deeper  into  the  substratum  as  the  age  of  the  culture  increases." 

It  is  significant  that  the  three  acid-forming  organisms  found  by 
Goadby,  in  the  deep  layers  of  carious  dentin,  do  not  form  pigment 
in  their  artificial  media. 

Fig.  364  Fig.  365 


Cervical  caries  associated  with  secondary  Caries  of  cementum  and  dentin  com- 

dentin.  Area  pigmented.  pletely  encircling  the  tooth. 

Caries  of  Cementum. — Caries  of  cementum  occurs  when  the  gum 
has  receded,  exposing  the  cementum  to  the  fluids  of  the  mouth.  As 
a  rule,  a  triangular  depression  exists  bounded  by  the  thickened  gum 
margin,  the  cementum,  and  the  enamel.  This  favors  the  collection 
of  the  bacterial  plaques,  and  caries  follows.  The  gum  may  be  much 
receded,  yet  no  caries  occurs.  As  a  rule,  however,  recession  and 
uncleanliness  frequently  assure  its  presence.  Especially  is  this  true 
in  cases  of  general  recession  in  aged  or  debilitated  persons. 

The  path  of  bacterial  invasion  after  decalcification,  is  by  way  of 
Sharpey's  fibers  to  the  lacunae  and  canaliculi;  later  the  dentin  is 
invaded  as  in  the  crown.  Frequently  the  form  of  the  cementum  is 
largely  retained,  while  the  decalcification  is  deep-. 


CLINICAL  HISTORY  385 

CLINICAL   HISTORY    OF    CARIES. 

The  clinical  history  of  dental  caries  records  the  observable  phe- 
nomena associated  with  its  inception,  progress,  and  termination. 

Inception  of  Caries. — Caries  begins,  after  the  manner  described 
in  the  pathology,  at  favoring  spots.  As  a  rule,  in  molars  the  occlusal 
fissures  are  first  decayed,  being  often  carious  in  this  situation  before 
fully  erupted.  Uninformed  parents  usually  consider  the  first  perma- 
nent molar  a  temporary  one,  and  frequently  neglect  it.  It  moreover 
has  often  seriously  defective  fissures,  which  afford  lodgement  for 
microbic  plaques,  which  seem  to  be  readily  formed  because  of  the 
unhygienic  state  of  the  temporary  teeth,  which  are  frequently 
carious,  and  the  permanent  molars  are  unbrushed  during  eruption. 
Not  infrequently  a  cavity  is  produced  on  the  mesial  surface  of  this 
tooth  by  a  carious  condition  of  the  distal  surface  of  the  second 
temporary  molar.  In  other  mouths,  both  teeth  are  afi^ected  alike, 
owing  to  the  nature  of  the  approximation.  The  relative  liability  of 
the  various  surfaces  of  the  different  teeth  to  caries  may  be  averaged 
for  a  great  number  of  persons,  but  tables  drawn  from  clinical  cases 
may  have  little  application  to  a  particular  individual,  as  peculiarities 
of  local  predisposing  causes  and  personal  habits  modify  the  inception. 
Nevertheless,  such  tables  are  exceedingly  interesting  as  showing  a 
general  relative  liability. 

The  following  is  from  the  U.  S.  Army  report,  70,000  teeth  being 
filled. 

Average  percentage 
Teeth.  of  each  carious. 

First  permanent  molars 6.5 

Second  permanent  molars  . 5.1 

Upper  central  incisors 3.9 

Premolars 2.8 

Third  molars ....2.0 

Upper  canines 1.7 

Lower  incisors ....0.7 

Lower  canines     .      . 0.5 

The  lower  anterior  teeth  are  the  last  of  all  to  be  affected,  and  it  is 
common  to  see  the  six  lower  anterior  teeth  free  from  caries,  years 
after  all  of  the  other  teeth  have  been  lost.  This  is  attributable  to 
the  constant  motion  of  the  saliva,  the  presence  of  calculus,  and  to 
the  mechanical  effects  of  tongue  movement,  lip  movement,  and 
mastication. 

In  the  temporary  set,  the  molars  decay  much  more  frequently  than 
the  incisor  teeth,  partly  because  longer  retained  and  partly  because 
of  the  width  of  their  approximations.    The  pulp  is  readily  exposed 
because  of  its  relatively  larger  size. 
25 


386 


DENTAL  CARIES 


Approximal  cavities  are  frequently  more  broad  than  deep,  and 
present  problems  of  anchorage. 

The  Progress  of  Caries. — The  rapidity  of  progress  of  caries  depends 

upon  the  intensity  of  the  action  of  the  exciting  cause,  the  structure 

of  the  tooth,  and  the  nature  of  the  vital  resistance  offered.     The 

exciting  cause  will  act  most  intensely  in  mouths  ill-cared  for,  and 

containing  much  carbohydrate  debris,  and  these  conditions  being 

equal,  enamel  of  poorer  organization  and  presenting  a  greater  degree 

of  solubility,  in  teeth  presenting  broad  approximations,  will  be  the 

more  rapidly  destroyed.     Caries  does  not  begin,  but  may  spread 

under  the  gum. 

Fig.  366 


Caries  undermining  enamel:  a,  masses  of  bacteria  lining  the  cavity.     X  50.     (Miller.) 


Williams  has  expressed  the  opinion  that,  as  a  rule,  the  process  of 
enamel  destruction  occupies  a  considerable  period  of  time,  a  fact 
which  may  account  for  the  general  lack  of  caries  in  the  temporary 
teeth  until  about  four  or  five  years  of  age. 

The  decalcified  enamel  may  retain  its  form  for  a  time  after  dentin 
decalcification  has  begun.  An  opaque  spot,  often  discolored,  is 
seen  upon  the  tooth,  and  is  readily  broken  down  by  an  instrument 


CLINICAL  HISTORY  387 

before  dentin  decalcification  occurs.  If  the  approximating  tooth  be 
extracted,  the  carious  process  may  cease,  owing  to  the  removal  of 
the  bacterial  plaque,  or  a  lack  of  food  supply  (retention).  This  result 
may  not  follow,  if  the  dentin  has  been  invaded  before  the  extraction. 

After  enamel  destruction  at  a  limited  area,  caries  progresses  along 
its  inner  side  and  penetrates  the  dentin.  The  enamel  is  undermined. 
The  extent  of  cavity  orifice  is  no  certain  guide  as  to  the  depth  of 
penetration.  The  under  surface  of  the  enamel  then  decalcifies.  This 
is  backward  or  secondary  decay  of  enamel,  and  causes  an  opaque 
appearance  of  the  undermined  enamel. 

Cases  are  frequently  observed,  in  which  the  only  external  evidence 
of  caries,  in  a  molar  or  bicuspid,  is  a  white  or  bluish-black  line  marking 
the  fissure,  and  yet  the  dentin  may  be  deeply  and  widely  penetrated 
(Fig.  367,  A). 

Fig.  367 
A  B 


As  a  rule,  however,  as  the  cavity  in  the  dentin  enlarges,  the  enamel 
at  the  orifice  becomes  disintegrated,  so  that  the  orifice  is  enlarged 
and  more  food  debris  enters  to  accelerate  the  process  (Fig.  353).  A 
deep  and  wide  cavity  may  thus  be  formed  before  the  patient  is 
objectively  or  even  subjectively  aware  of  its  existence.  After  a 
time,  the  occlusal  enamel  boundary  of  the  cavity  breaks  down  and 
food  is  even  more  readily  admitted. 

It  has  been  noted  that  if  the  enamel  break  away  in  such  a  manner 
as  to  expose  the  carious  dentin  to  the  friction  of  food  masses  which 
are  not  retained  and  to  the  access  of  saliva,  the  progress  of  the 
caries  is  delayed  and  in  some  cases  ceases  altogether.  The  process 
of  eburnation  is  set  up.  (See  Transparent  Zone  and  Tubular 
Calcification.)     (Fig.  367,  B.) 

The  process  is  sometimes  seen  in  certain  cases  in  which  caries 
has  followed  the  dento-enamel  junction,  the  enamel  chipping  off 
as  undermined,  so  that  almost  the  entire  superficial  portion  of  the 
dentin  may  be  subjected  to  this  process  and  remain  of  original  form 
and  discolored  and  eburnated.  This  is  "spreading  caries."  In 
other  cases  the  tubules  are  followed  and  the  pulp  is  rapidly  ap- 
proached.   This  is  "penetrating  caries"  (Fig.  345). 


388  DENTAL  CARIES 

Caries  may  progress  rapidly  for  a  period,  and  then  receive  a  check 
to  its  progress.  Teeth  previously  free  from  the  disease  may  suddenly 
fall  victims  to  its  rapid  and  widespread  progress.  No  doubt,  in  many 
of  these  cases,  there  are  removed  from  or  added  to  the  local  oral 
conditions,  constitutional  influences  which  deter  or  favor  the  local 
development  of  caries  producing  bacteria.  The  editor  has  the  models 
of  the  jaws  of  a  boy,  aged  fourteen  years,  with  every  tooth  but  three 
decayed  to  the  gum,  and  the  three  teeth  contained  six  cavities. 

Secondary  dentin  is  less  readily  decalcified  than  primary  dentin. 

The  dentin  of  pulpless  teeth  is  more  rapidly  invaded  after  enamel 
decalcification  than  that  of  vital  teeth,  owing  to  the  absence  of  vital 
resistance.  This  condition  does  not  necessarily  apply  to  the  enamel 
of  pulpless  teeth. 

While  caries  appears  at  all  ages  from  childhood  to  old  age,  its 
ravages  are  most  pronounced  and  its  progress  most  rapid  during  the 
period  of  adolescence  and  early  maturity.  Its  effects  are  most 
marked  between  the  ages  of  eight  and  twenty-five  years.  As  a  rule, 
a  denture  which  remains  at  twenty-five  years  unaffected  by  caries, 
remains  unaffected  or  but  slightly  affected  to  an  indefinite  age.  To 
be  sure,  this  implies  two  conditions:  (1)  That  the  active  causes  of 
caries  have  been  in  but  slight  evidence,  and  (2)  that  the  denture  is 
of  the  highest  order.  The  classes  of  dentures  which  escape  are  per- 
fectly formed  and  symmetrically  arranged  teeth,  in  the  mouths  of 
patients  who  lead  sanitary  lives  and  care  for  the  teeth,  who  masticate 
vigorously,  and  who  escape  other  diseases.  Very  filthy  dentures 
may  escape,  owing,  as  stated,  to  putrefaction.     (See  p.  361.) 

Caries  beginning  at  the  junction  of  the  cementum  and  enamel  of 
the  teeth  has  a  somewhat  different  clinical  history  from  that  noted 
when  its  occurrence  is  in  other  situations.  Its  progress  is  subject  to 
great  variations.  In  any  of  the  catarrhal  conditions  or  atrophic 
conditions  of  the  gum  which  lay  bare  the  neck  cementum,  caries 
usually  occurs.  It  occurs  also  as  a  process  secondary  to  labial 
abrasion  and  erosion  of  the  teeth.  Teeth  affected  by  erosion,  however, 
at  the  ended  area  are  commonly  exempt  from  dental  caries. 

The  Terminations  of  Caries. — After  the  pulp  is  exposed,  it  sooner 
or  later  becomes  inflamed  and  hypertrophies  or  dies.  In  the  latter 
case  putrefaction  results,  which  for  a  time  may  exert  a  restraining 
influence  upon  decay,  but  not  for  a  long  time. 

Masses  of  food  freely  enter  the  pulp  cavity  and  caries  proceeds  in 
the  dentin  from  within  toward  the  periphery.  This  is  "secondary 
caries"  of  dentin,  and  as  it  occurs  in  dentin  without  vitality,  no 
transparency  results  (Fig.  362).  Notwithstanding,  caries  at  this 
stage  proceeds  rather  slowly,  particularly  if  the  crown  be  much 


CLINICAL  HISTORY  389 

broken  down.  The  result  of  secondary  caries  is  a  hollowing  out  of 
dentin  of  the  root,  and  finally  a  decalcification  of  the  cementum, 
which  may  persist  for  some  time  as  a  thin,  elastic  wall.  Finally  this 
is  destroyed  either  at  the  occlusal  periphery,  or  caries  causes  pene- 
tration to  the  pericemental  tissue.  This  may  occur  laterally  or 
through  to  the  bifurcation  of  the  roots.  In  either  case  it  is  called 
"perforation  by  caries."  Into  this  perforation  the  pericemental 
tissue  may  become  protruded  by  hypertrophy,  and  the  condition 
of  hyperplastic  or  fungous  gum  be  established.  Following  the 
breaking  down  of  the  crown,  the  blood  pressure  in  the  pericementum 
begins  an  extrusive  process,  the  pericementum  becomes  thickened, 
and  the  tooth  is  somewhat  loosened. 

Decay  of  the  root  face  and  interior,  and  breakage  of  the  cemental 
margins  proceed  simultaneously  with  the  extrusion,  until  finally  but 
a  small  discolored  bit  of  the  root  end  lies  upon  the  surface  of  the 
gum,  from  which  it  is  removed  by  some  slight  force  or  is  extracted. 

The  entire  process  of  caries  in  a  tooth  may  thus  extend  over  a 
period  of  from  ten  to  twenty  years. 

At  times  the  extrusive  force  pushes  a  root  up  sidewise,  particularly 
when  the  tooth  has  been  tipped  over  before  the  loss  of  the  crown. 
It  may  thus  be  retained  in  position  and  attached  upon  its  under  side 
for  some  time.  The  upper  side  may  be  polished  by  abrasion.  The 
exposed  end  of  a  root  undergoing  extrusion  is  also  sometimes  made 
smooth  by  abrasion.  A  bit  of  root  left  in  situ  after  breakage  during 
extraction  usually  undergoes  the  same  process  of  extrusion,  but  may 
not  decay  until  it  comes  under  oral  influences.  Usually  a  sinus  leads 
to  such  a  root,  but  very  rarely  the  gum  may  heal  over  it. 

Such  a  root  may  at  any  time  become  the  source  of  apical  abscess 
or  of  an  intractable  neuralgia,  the  cause  being  only  determinable 
by  radiography. 


CHAPTER  XIII. 

DENTAL  CARIES:  DIAGNOSIS,  SYMPTOMS,  AND 
PROGNOSIS. 

HYPERSENSITIVE   DENTIN   AND   ITS    THERAPEUTICS. 

Diagnosis  of  Dental  Caries. 

The  diagnosis  of  dental  caries  is  made  through  both  objective  and 
subjective  symptoms.  The  signs  are  the  existence  of  cavities  and 
of  softened  areas,  directly  visible  or  made  evident  through  instru- 
mental means.  The  symptoms  are  pains  of  several  degrees  of  inten- 
sity. The  nature  and  intensity  of  the  pains  furnish  a  guide  to  the 
depth  of  the  carious  invasion,  and  but  an  indirect  indication  of  the 
location  of  the  disease. 

Diagnosis  by  Objective  Symptoms. — The  presence  of  the  markings 
of  superficial  decay,  decalcified  surfaces,  or  cavities  may  often  be 
detected  at  a  glance  or  be  seen  reflected  in  a  mouth  mirror.  Opacity 
of  enamel  is  usually  due  to  its  superficial  decalcification  or  caries 
beneath  it,  though  at  times  a  malformation  may  exist.  Sometimes 
a  zinc  phosphate  lining  will  cause  an  opacity  resembling  backward 
caries  of  enamel.  The  discoloration  or  opacity  about  a  fissure  should 
excite  suspicion  of  caries.  In  the  routine  examination  for  cavities, 
sharp,  finely  pointed  explorers  bent  at  various  angles  are  to  be  passed 
over  all  the  surfaces  of  the  teeth.  If  the  enamel  at  any  point  admit 
the  point  of  the  explorer,  caries  is  usually  present.  Fissures  are 
sometimes  deceptive  in  this  respect.  A  good  rule  is  to  adjudge  the 
presence  of  caries  when  the  point  catches  slightly  as  removed.  It 
is  well  to  remember  in  this  connection,  that  an  unsuspected  adjunct 
fissure  will  often  contain  beneath  it  caries  deeper  than  the  central 
point  judged  defective. 

In  the  search  for  approximal  caries  great  care  is  required,  explorers 
with  very  short  points  being  often  necessary,  as  long  points  will  not 
turn  into  the  cavity  owing  to  the  close  contact.  The  ordinary  No.  7 
explorer  has  not  a  short  enough  tine.  Frequently  a  cavity  may 
only  be  discoverable  from  one  point  of  access,  so  that  the  approximal 
surfaces  should  be  examined  both  from  the  labial  and  lingual  sides. 
In  the  absence  of  evident  cavities,  some  force  should  be  applied  to 
( 390 ) 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     391 
Fig.  368  Fig-  369 


Explorer 
for  caries. 
(Jack.i) 


Dow  electric  lamp  for  mouth  illumination,  with 
reflectors.  Reflector  A  is  jointed  to  vary  the  angle  of 
reflection.  Reflector  B  is  for  illumination  of  the 
fauces.  Reflector  C  is  for  lateral  illumination. 
(Jack.2) 

detect  softened  spots  of  enamel.  The 
catching  of  the  explorer  upon  both  teeth, 
after  it  has  passed  through  the  interspace, 
often  simulates  the  catch  in  a  cavity. 

Unwaxed  floss  silk  passed  over  carious 
surfaces  indicates  a  rough  surface  by 
fraying.  It  may,  however,  at  times  pass 
readily  over  a  cavity  easily  detected  by 
instruments;  so  that  it  is  not  absolutely 
reliable  as  a  test.  It  also  catches  on  a 
rough  filling  or  protruding  filling  margin. 
If  the  short,  sharp  pain  of  hypersensitive 
dentin  is  produced  as  floss  passes  between 
the  contact  points  of  the  teeth,  either  a 
masked  small  cavity  or  a  loose  filling 
should  be  suspected,  and  if  not  found 
with  the  explorer  or  light,  a  wedge  should 
be  introduced. 

The  strong  light  of  an  electric  mouth 
lamp  transmitted  through  the  teeth  ex- 
hibits a  cavity  as  an  opaque  spot  outlined 
upon  a  pinkish  background.  It  not  only 
permits  an  easy  diagnosis,  but  also  affords 
evidence  of  the  depth  of  penetration. 
Mechanical  separators  or  wedges  are  at 
times  necessary  to  press  apart  contiguous 
teeth  sufl^iciently  to  admit  exploring  in- 
struments. 


1  American  Text-book  of  Operative  Dentistry. 


2  Ibid. 


392  DENTAL  CARIES 

The  necks  of  the  teeth  should  be  examined  with  sharp  points,  to 
note  any  softness  of  the  tooth  tissues.  The  margins,  particularly 
the  cervical  and  neighboring  margins,  of  every  filling  should  be 
explored  to  test  the  integrity  of  the  junction  of  filling  and  tooth, 
or  any  excess  or  deficiency  of  filling  material. 

The  examination  should  be  conducted  by  one  of  two  systematic 
methods.  In  one  method  the  occlusal  faces  of  all  the  teeth  are  first 
examined  in  one  survey,  then  the  interproximal  spaces,  and  lastly, 
the  buccal  and  lingual  surfaces  of  the  teeth.  In  the  other  method, 
every  portion  of  each  tooth  is  examined,  beginning  with  a  central 
incisor  or  terminal  molar,  before  passing  to  the  adjoining  tooth.  Any 
cavity  or  condition  found  should  be  noted  upon  a  diagram  for  refer- 
ence at  sittings. 

Diagnosis  by  Subjective  Sjrmptoms. — Complaints  by  patients 
that  cold  or  hot,  salt,  sweet,  or  acid  substances  taken  into  the  mouth 
cause  unlocalized  or  partly  localized  pain,  indicate  exposed  and 
hypersensitive  dentin  or  pulp  exposure.  Such  complaint  is  to  have 
due  consideration.  Slight  pain  has  also  been  produced  by  the 
passage  of  floss  over  a  minute  cavity  unexplorable  before  wedging, 
and  is  probably  due  to  compression  of  liquid  upon  dentine.  This 
symptom  at  the  cervix  of  a  tooth  indicates  hypersensitive  exposed 
dentin. 

Pain  beginning  without  the  application  of  special  stimuli,  is  like- 
wise ordinarily  connected  with  caries  or  its  sequelae,  and  should  be 
taken  into  account. 

Pain  produced  upon  mastication  has  either  the  significance  of 
pressure  on  fibrils  or  pulp,  or  is  a  symptom  of  pericemental  irritation. 

Prognosis  of  Caries. 

If  existing  caries  be  promptly  treated  in  youth  and  a  proper  sys- 
tematic prophylaxis  be  employed,  its  recurrence  during  youth  may 
be  largely  prevented.  At  about  adult  age  a  fair  degree  of  immunity 
may  be  expected.  In  the  absence  of  treatment  or  prophylaxis,  the 
exciting  causes  seem  to  become  very  active,  and  many  teeth  may  be 
lost  from  caries  or  by  reason  of  extraction  for  pulp  and  pericemental 
diseases.    Extraction  itself  brings  many  evils  in  its  train. 

Even  advanced  caries  may  be  checked  by  proper  filling  or  crown- 
ing, and  if  then  prophylaxis  receive  due  attention,  the  prognosis 
for  the  teeth  is  generally  good;  indeed,  it  seems  as  though  but  few 
conditions  exist  dependent  upon  caries  alone,  which  are  not  subject 
to  correction  by  some  of  the  means  within  the  resources  of  the 
profession. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     393 


Hypersensitivity  of  Dentin. 

The  exposure  of  dentin  to  external  agencies  is  so  commonly 
followed  by  an  increase  in  sensitivity,  that  the  condition  requires 
description  in  itself.  It  is  a  general  condition  attendant  upon 
abrasion,  erosion,  and  caries,  and  has  a  therapeutics  of  its  own. 

The  term  sensitive  dentin  applied  to  this  condition  is  a  misnomer; 
all  vital  dentin  is  sensitive,  and  its  degree  of  sensitivity  differs 
markedly  in  individuals;  it  is  only  when  hypersensitivity  is  observed 
that  the  condition  becomes  pathological. 

Hypersensitivity  of  dentin  may  be  defined  as  such  a  degree  of 
sensitiveness  of  the  dentinal  fibrils,  as  interferes  with  the  comfortable 
excavation  and  shaping  of  a  cavity  of  decay ;  or  which,  in  the  absence 
of  dental  ministrations,  causes  painful  symptoms,  as  a  rule,  reflected 
about  neighboring  parts. 

Causes  and  Pathology. — Normally  the  dentin  is  protected  from 
external  agencies  by  the  enamel,  and  in  the  early  stages  of  gum 
recession  by  the  cementum,  though  it  has  been  shown  that  in  some 
cases  the  dentin  is  not  covered  by  either.     (See  p.  182.) 

With  the  removal  of  these  coverings  by  caries,  erosion,  abrasion,  or 
fracture,  the  terminal  filaments  of  the  dentinal  fibrils  become  sub- 
jected to  sudden  variations  of  temperature,  ranging  from  a  little 
above  32°  F.,  the  temperature  of  ice-water,  to  130°  F.,  that  of  very 
hot  foods  or  liquids. 

These  thermal  stimuli  at  times  give  evidence  of  their  eflfect  by 
producing  painful  sensations.  The  pulp  is  stimulated  through  the 
odontoblasts  and  their  relations  with  the  terminals  of  sensory  nerves 
in  the  pulp,  and  a  degree  of  vascular  overfulness  occurs  which  may 
be  denominated  mild  hyperemia.  The  effect  of  these  reactions  is  to 
cause  the  sensory  functions  of  the  pulp  to  become  somewhat  exalted, 
and  it  therefore  becomes  more  responsive  to  the  stimuli. 

Apart  from  the  effect  of  thermal  changes,  other  substances  act  as 
irritants.  The  lactic  acid  and  other  bacterial  products  in  the  cavity 
of  decay,  without  doubt  play  a  part  in  exalting  the  irritability  of  the 
fibrils.  A  slightly  loosened  filling  holds  the  acid  in  contact,  as  such 
cases  are  often  very  sensitive.  Salt,  sweet,  or  acid  substances  intro- 
duced into  the  mouth  are  also  evidently  irritant,  as  active  symptoms 
follow  their  application  to  hypersensitive  dentin. 

Mechanical  abrasion  or  erosion  may  irritate  the  fibrils,  or  at  least 
expose  them  to  the  action  of  other  irritants.  As  a  rule,  however,  the 
abraded  or  eroded  surfaces  are  protected  from  hypersensitivity  by 
the  process  of  eburnation.     (See  Transparent  Zone.) 


394  DENTAL  CARIES 

The  scraping  of  necks  of  teeth  with  scalers  sometimes  induces 
exposure  of  dentin.  Within  cavities  of  decay,  the  hypersensitivity 
is  greatest,  as  a  rule,  at  the  dentinal  periphery.  That  at  this  point 
the  dichotomous  endings  of  the  tubules  present  a  greater  number 
of  fibrils  to  the  action  of  the  irritant  is  quite  evident  (Fig.  117). 

In  cervical  hypersensitivity,  the  cementum  or  enamel  is  removed 
by  abrasion,  erosion,  or  caries,  and  the  fibrils  are  exposed.  The 
presence  of  the  granular  layer  of  Tomes  in  this  situation,  and  the 
possibility  of  this  layer  containing  the  expansions  of  the  fibrils,  are 
to  be  considered. 

In  certain  cases,  the  irritation  excited  by  the  touch  of  an  instrument 
to  dentin  adjacent  to  enamel  is  carried  to  the  pulp  by  anastomosing 
dentinal  fibrils.  This  was  proved  by  a  few  cases,  of  which  the  follow- 
ing is  an  extreme  one : 

In  a  central  incisor,  secondary  dentin  had  filled  a  portion  of  the 
pulp  cavity  (Fig.  370,  »S  D).    Caries  had  subsequently  removed  the 

incisal  portion  of  this  secondary  growth  and 
^^°-  ^''^  also    the  dentin   containing  fibrils    leading 

from  the  pulp  cavity  to  the  middle  of  the 
incisal  edge.  The  application  of  an  ex- 
cavator to  dentin  in  the  incisal  portion  of 
the  cavity  (at  A),  the  fibrils  of  which  could 
have  no  direct  relation  with  the  pulp,  pro- 
duced flashes  of  pain.  This  was  unmistak- 
ably of  the  character  of  hypersensitive 
dentin. 

A  professional  friend  claimed  to  feel  sen- 
seL'l'lTonL\™ThTper-  f i^ivity  in  a  ccrvicolingual  cavity  of  a  molar, 
sensitive  dentin:  5:  D,  sec-  in  which  the  filaments  had  been  destroyed 
hyJersensltivi'ty^'  """TDia-  ^y  suppuration  for  one-third  of  the  length 
grammatic.)  of  the  canals.    If  his  contention  was  true, 

the  sensation  must  have  been  conducted 
by  way  of  the  granular  layer  of  Tomes  to  the  level  of  the  pulp, 
and  thence  by  the  fibrils  to  its  substance.     (See  Fig.  126.) 

Spots  of  cervical  hypersensitivity  have  been  occasionally  recorded 
as  occurring  in  teeth,  the  canals  of  which  have  been  filled. 

Head"^  records  a  case  in  which  the  dentin  bounding  the  pulp  canal 
remained  hypersensitive  for  a  year  after  the  pulp  was  removed.  In 
this  connection  the  possibility  of  the  presence  of  a  vital  pulp  filament 
in  the  pulp  canal,  or  of  irritable  apical  tissue  receiving  the  impact  of 
liquid  forced  down  upon  it  by  a  canal  probe,  or  of  a  pericementum 

1  Dental  Cosmos,  1899. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     395 

irritable  to  touch  of  any  sort,  must  all  have  due  differentiation.  I 
have  never  seen  a  case  of  hypersensitivity  of  dentin  in  which  some 
filament  of  pulp  was  not  present,  in  at  least  a  part  of  the  tooth. 

Dentin  cannot  become  inflamed  in  the  ordinary  sense,  as  leukocytes 
cannot  enter  the  tubules;  nevertheless,  the  irritability  of  the  fibrils, 
like  that  of  other  protoplasm,  may  be  exalted  (or  lessened).  It  has 
been  noted  that  during  excavation  of  a  cavity  the  irritability  is,  as 
a  rule,  greatest  at  the  surface  of  the  dentin — i.  e.,  at  the  point  at 
which  irritants  are  present  in  greatest  amount,  and  the  fibrils  most 
numerous. 

With  hypersensitivity  other  functions  are  increased,  and  in  con- 
ditions producing  a  constant  stimulation,  a  constructive  change  may 
occur  and  the  fibrils  form  tubular  substances  at  their  own  expense. 
(See  Transparent  Zone  and  Tubular  Calcification.) 

That  the  hypersensitivity  is  primarily,  as  a  rule,  a  disease  of  the 
fibrils  involved,  or  of  the  fibrils  and  their  odontoblasts  is  shown  by 
the  fact  that  occasionally  of  two  cavities  in  the  same  tooth,  one  will 
present  a  hypersensitivity  and  another  none;  again,  one  part  of  a 
cavity  may  be  hypersensitive  and  the  rest  not  so.  In  other  cases, 
perfectly  normal  dentin  is  hypersensitive,  as  noted  when  the  attempt 
is  made  to  reduce  a  sound  tooth  for  bridge-work,  or  a  sound  fissure 
is  opened  for  prevention  of  decay. 

There  have  been  two  theories  accounting  for  the  transmission  of  the 
impulse  which  is  translated  by  the  patient  as  pain:  (1)  That  a  con- 
contraction  of  the  whole  cell,  fibril  and  odontoblast,  occurs,  the  sen- 
sory nerve  endings  being  pressed  upon  in  the  act — i.  e.,  contraction 
causes  a  lateral  increase  in  size.  (2)  That  a  wave-like  motion  along 
the  protoplasm  is  set  up,  causing  excitation  of  the  sensory  nerves 
and  due  to  the  incompressibility  of  the  water.     (Gysi.) 

The  first  is  analogous  to  the  contraction  of  a  voluntary  muscle 
cell  under  nerve  impulse.  The  whole  muscle  cell  contracts,  though 
the  nerve  ending  is  supplied  to  only  a  portion  of  it.^  This  hypoth- 
esis fits  the  symptoms  as  excited  by  both  mechanical  and  chemical 
irritants,  while  the  second  theory  does  not.  If  the  contention  of 
Robertson  that  the  odontoblast  is  connected  with  the  axis  cylinders 
of  the  nerves  be  true,  then  the  contraction  pulls  the  nerve  fibril. 

If  Mummery  is  correct  in  his  statement  that  nerve  fibres  enter 
the  tubules  and  end  at  their  subenamel  terminals,  then  even  this 
theory  must  be  modified,  as  the  irritation  will  be  direct.  The  con- 
traction may  still  be  possible.     (See  p.  181.) 

'  Black:  American  System  of  Dentistry. 


396  DENTAL  CARIES 

Symptoms. — A  certain  degree  of  uneasiness  of  undefined  character 
may  at  times  be  noted  in  teeth  containing  cavities,  but,  as  a  rule, 
pain  other  than  pulp  pain  is  only  felt  upon  the  application  of  special 
stimuli.  Of  course,  the  presence  of  ferments,  acids,  etc.,  in  a  cavity 
are  real  stimuli. 

The  infiltration  of  acid,  salt,  or  sweet  substances  into  contact  with 
a  hypersensitive  surface  is  followed  by  a  wave  of  gnawing  pain, 
reflected  usually  along  the  course  of  contiguous  nerve  filaments. 
While  not  definitely  localized,  owing  to  the  fact  that  the  pulp  does 
not  possess  a  tactile  or  localizing  sense,  the  pain  may  usually  be 
referred  to  a  certain  part  of  the  mouth.  The  pressure  of  an  instru- 
ment upon  the  dentin  is  attended  by  a  flash  of  sharp  pain,  which 
continues  for  a  time,  but  lessens  if  the  contact  be  maintained.  In 
this  test  the  pain  is  localized  in  the  affected  tooth,  the  touch  of  the 
instrument  being  followed  by  a  recognition  of  position  by  the  tactile 
organ  of  the  tooth,  the  pericementum. 

Occasionally,  food  forced  by  mastication  against  a  hypersensitive 
surface,  such  as  due  to  abrasion  or  caries  in  a  crevice,  will  produce 
a  sharp  pain  subsiding  promptly,  and  which  may  not  be  repeated  for 
some  time.  The  mere  rubbing  together  of  opposing  abraded  surfaces 
may  cause  the  symptom,  and  is  more  pronounced  if  a  hard  sub- 
stance, as  grit  gets  between  them. 

Cavities  dried  for  filling  usually  produce  a  steady  pain,  caused  by 
dryness  and  relieved  by  an  analgesic  or  by  filling. 

It  is  beyond  doubt  that  individuals  differ  as  to  the  degrees  of 
normal  dentinal  sensitivity;  the  dentin  of  one  person  may  be  cut 
freely  without  evidence  of  marked  pain;  in  another,  the  touch  of  an 
instrument  to  the  newly  exposed  dentin  is  productive  of  unbearable 
pain.  The  difference  in  degree  of  irritability  is  manifested  in  another 
manner:  If  a  mild  sedative — for  example,  oil  of  cloves  or  an  obtun- 
dent— be  applied  to  the  hypersensitive  dentin  of  one  person,  it  may 
remove  the  distressing  symptoms,  but  with  others  it  may  be  necessary 
to  employ  the  most  extreme  measures  to  reduce  in  any  degree  the 
hypersensitivity.  In  some  cases,  the  exposure  of  dentin  about  the 
necks  of  teeth  may  induce  such  an  unbearable  local  pain  or  neuralgic 
condition  as  to  positively  demand  relief. 

In  a  few  cases  enamel  has  exhibited  sensitivity.  In  one  case  the 
effort  to  open  sound  fissures  about  a  cavity  for  prevention  excited 
sharp  pain,  ceasing  upon  removal  of  the  instrument.  The  patient 
was,  hiowever,  a  sufferer  from  insomnia,  and  from  the  effects  of 
morphine  taken  for  it,  and  her  dentin  was  exquisitely  sensitive.  The 
same  phenomenon  of  enamel  sensitivity  is  to  be  noted  in  one  of  her 
children. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     397 

In  another  patient,  the  side  of  the  enamel  exposed  by  a  cavity  in  a 
molar  analogous  to  that  in  Fig.  370  gave  flashes  of  pain  when  touched 
with  an  excavator  point,  though  no  evident  direct  path  of  trans- 
mission to  the  pulp  could  be  seen.  Caush's  tubes  and  indirect  trans- 
mission seem  the  only  basis  of  explanation.     (See  Fig.  179.) 

There  is  a  pseudohypersensitivity  of  enamel  in  some  cases,  due  to 
apprehension.  The  patients  can  be  ridiculed  out  of  the  idea  by 
demonstrating  its  absurdity,  as,  for  example,  by  touching  a  cusp 
and  then  showing  them  the  part  touched.  Pericemental  irritability 
at  times  must  also  be  excluded. 


Fig.  371 


Fig.  372 


The  Teter  nitrous  oxide  and 
oxygen  apparatus  on  apparatus 
stand. 


Gregg  nasal  inhaler. 


There  can  be  no  question  that  systemic,  nervous  irritability  from 
any  cause  aggravates  the  phenomenon  of  hypersensitivity,  though 
whether  it  can  make  dentin  more  sensitive,  or  whether  the  patient 
is  less  able  to  endure  pain,  is  not  clear. 

The  general  perceptivity  of  the  individual  seems  to  play  a  part, 
and  even  apparently  normal  dentin  may  be  exquisitely  hypersen- 
sitive.    Again,   pain  produced  in  excavation  may  be  due  to  the 


398  DENTAL  CARIES 

character  of  the  manipulation,  heavy  continued  burring  producing 
heat;  hghter  touches  may  excavate  equally  well,  but  produce  much 
less  pain.    The  dulness  of  the  excavator  or  bur  has  a  similar  effect. 

Diagnosis. — In  the  diagnosis  the  above  characteristic  symptoms 
are  to  be  considered.  The  decisive  test  is  made  by  pressing  an 
instrument  upon  the  suspected  surface,  when  the  characteristic  pain 
is  produced,  subsiding  upon  or  shortly  after  removal  of  the  contact. 

Upon  the  pulpal  wall  of  deep  cavities  doubt  may  exist  as  to 
whether  the  pain  is  due  to  pulp  irritation. 

A  suspected  exposure  may  be  differentiated  by  the  localization  of 
the  pain  upon  touch,  to  a  point  corresponding  to  the  pulp  horn  or 
pulp  body,  or  by  the  point  catching  in  the  exposure.  Hypersensitive 
dentin  will  be  more  generally  distributed  or  occur  at  points  at  which 
exposure  is  impossible.  Pulp  abnormality  or  approach  may  be 
detected  by  means  of  a  drop  of  cool  water  or  a  blast  of  cool  air  from 
a  syringe.    (See  Hyperemia  of  the  Pulp.) 

Treatment. — The  methods  of  treatment  which  have  been  followed 
for  the  relief  of  hypersensitivity  of  dentin,  and  the  induction  of  such 
a  degree  of  analgesia  as  will  permit  the  necessary  cutting  of  dentin, 
may  be  divided  into  general  and  local. 

General  Remedies. — The  general  remedies  employed  are  those 
which  abolish  or  lessen  the  perceptive  function  in  the  centres  of  the 
fifth  pair  of  nerves,  or  which  reduce  hyperirritability  of  the  nervous 
system.  Either  general  anesthesia  or  general  anodynes  are  em- 
ployed to  lessen  perception.  The  inhalation  of  a  few  whiffs  of  chloro- 
form or  ethylic  ether  lessens  the  perception  of  pain,  or  a  mixture  of 
chloroform,  ether,  and  alcohol  may  be  used.  Chloroform  is  usually 
avoided  in  this  connection  on  account  of  its  dangers  when  used  in 
the  sitting  position.  Slight  etherization,  the  inhalation  being  carried 
only  to  the  benumbing  point,  affords  marked  relief  from  the 
pain  incidental  to  the  cutting  of  hypersensitive  dentin.  Nitrous 
oxide  and  oxygen  administered  to  the  point  at  which  "analgesia" 
without  anesthesia  occurs  is  a  method  now  much  employed.  A 
special  nasal  inhaler  admits  the  gases  in  various  combinations, 
the  mixture  of  the  prepared  gases  being  made  in  the  mixing 
chamber  of  the  apparatus,  after  the  gases  leave  the  cylinders. 

It  is  preferable  that  the  gases  be  warmed  to  avoid  the  irritation 
of  the  lungs  by  the  cold  gases,  though  for  short  operations  this  is 
often  omitted. 

Rebreathing  the  carbon  dioxid  and  gases  exhaled  is  also  advocated 
as  a  respiratory  stimulant  and  for  economy.  In  view  of  hypersensi- 
tive dentin  the  method  is  now  routine  for  cavity  preparation  and 
for  the  grinding  of  teeth  with  living  pulps,  for  abutments  or  for  other 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     399 

work  involving  a  reasonable  amount  of  pain.  It  is  not  generally 
useful  for  pulp  removal  unless  complete  anesthesia  is  induced.  The 
method  has  various  dangers  which,  while  not  preventing  its  use  in 
careful  hands,  renders  it  not  to  be  carelessly  employed.  Fear  is  apt 
to  contra-indicate  its  use  in  children. 

The  element  of  suggestion  and  confidence  on  the  part  of  the 
operator  seems  to  play  an  important  part  in  the  success  of  the  anal- 
gesia, though  the  analgesia  is  not  dependent  upon  it.  The  patient 
is  able  to  cooperate  with  the  operator,  not  having  lost  consciousness. 
In  the  practical  application  of  the  mixed  gases,  the  apparatus  is  first 
set  as  to  constancy  of  flow  of  both  gases,  the  proportion  of  95  per 
cent.  N2O  and  5  per  cent.  O  being  first  applied,  until  the  patient 
reaches  a  condition  of  somnolence,  of  which  he  informs  the  operator. 
The  proportions  are  now  changed  until  approximately  80  per  cent. 
N2O  and  20  per  cent.  O  are  being  given,  though  this  proportion 
is  variable.  The  patient  is  instructed  to  breathe  through  the  nose  if 
pain  is  felt,  thus  obtaining  deeper  analgesia.  Conversely,  as  work  is 
not  being  done,  he  may  breathe  through  the  mouth.  If  greater  depth 
of  anesthesia  is  required,  the  exhaling  valve  which  ordinarily  vents 
the  expirations  is  adjusted  and  the  patient  then  rebreathes  the 
gases  together  with  his  own  carbon  dioxid,  which  further  stimulates 
respiration  and  gradually  passes  into  anesthesia,  especially  if  the 
percentage  of  oxygen  be  decreased.  Without  rebreathing,  95  per 
cent.  N2O  and  5  per  cent.  O  will  produce  anesthesia.  The  amount  of 
rebreathing  is  controlled  by  a  valve.  Somnoform  has  also  been  used 
with  a  special  inhaler  (De  Ford  or  Starck)  to  produce  analgesia. 

The  administration  of  general  anodynes,  particularly  the  com- 
bination of  morphin  and  atropin,  has  been  found  useful  in  this  field. 

I^ — Morphinae  siilph gr.  i 

Atropinse  sulph gr.  j-|q 

M.  etft.  pil.  No.  1. 

Sig. — To  be  taken  one-half  hour  before  operation. 

Flagg  noted  that  blondes  bear  morphin  sulphate  better  than 
brunettes;  particularly  are  nervobilious  and  bilionervous  patients 
idiosyncratically  opposed  to  its  use,  the  physiological  action  of  the 
drug  being  reversed  or  the  after-effects  being  pronounced.  Patients 
having  dark  hair  and  blue  eyes  may  be  expected  to  be  thus  idio- 
syncratic. For  them,  he  recommended  morphin  bimeconate  solution 
in  doses  equivalent  to  |  grain  of  the  salt,  to  be  taken  one  the  evening 
before,  and  the  other  before  the  operation. 

1  For  details  of  apparatus  and  application  read  C.  K.  Teter,  Dental  Cosmos,  August 
1912;  W.  C.  Teter,  Dental  Brief,  August,  1911;  A.  E.  Smith,  Items  of  Interest, 
December,  1913;  Harold  B.  Clark,  Items  of  Interest,  April,  1914,  and  others. 


400  DENTAL  CARIES 

Chloral  in  5  or  10  grain  doses,  administered  in  water  before  the 
operation,  has  a  quieting  effect  upon  the^ nervous  system.  Ambler^ 
has  suggested  the  use  of  from  10  to  20  drops  of  fluidextract  of  piscidia 
erythrina,  to  be  administered  about  ten  minutes  before  operating. 
Drowsiness  may  be  expected.  Phenobromate,  10  grains,  before 
operation,  or  15  grains  for  any  great  pain,  may  be  administered  in  a 
copious  draught  of  water. 

For  the  reduction  of  excitement  and  nervousness  in  anticipation 
of  dental  operation,  bromural,  5  grs.,  ordinarily  to  be  administered 
while  waiting,  or  10  grs.  in  unusual  cases,  is  highly  recommended  for 
this  purpose  by  Hecker.^  It  is  also  useful  in  insomnia,  and  its 
associated  hyperesthesia.  Quinine  sulphate,  5  grains  a  half-hour 
before  operation,  or  better  if  preceded  by  another  dose  the  day 
before  it  has  been  used. 

Hyoscyamin  hydrobromate,  eV  grain,  will  be  useful  in  those  cases 
which  are  associated  with  muscular  spasm  or  hysteria. 

The  coal-tar  derivatives,  phenacetin,  acetanilid,  and  others,  are 
occasionally  efficient.  The  preparation  known  as  antikamnia  (said 
to  be  a  combination  of  acetanilid,  caffein  citrate,  and  sodium  bicar- 
bonate) and  ammonol  (acetanilid  and  ammonium  carbonate,  equal 
parts)  are  to  be  preferred  in  this  connection.  The  dose  of  the  latter 
two  is  10  grains,  administered  one-half  hour  before  operation. 

The  induction  of  the  hypnotic  state  belongs  in  the  category  of 
means  acting  upon  the  nerve  centres.  The  use  of  the  ordinary 
suggestion  that  the  work  will  not  be  unduly  painful,  considerate 
treatment,  patience,  and  the  employment  of  remedies  all  have  a 
calming  influence,  permitting  relaxation  upon  the  part  of  the 
patient,  who,  if  "keyed  up"  to  expect  great  pain,  will  expect  and 
feel  unduly. 

The  use  of  blue-light  anesthesia  consists  in  causing  the  patient  to 
gaze  intently  for  a  few  minutes  at  a  blue-globed  electric  light  having 
a  reflector  behind  it.  A  blue  veil  is  thrown  about  the  head  and  lamp 
to  exclude  daylight.  Short  operations  have  been  performed  under 
its  sedative,  or,  possibly,  hypnotic  effects,  though  it  seems  to  fail 
in  some  cases. 

Local  Treatment.^ — The  local  treatment  of  hypersensitive  dentin 
may  be  considered  from  two  standpoints,  according  to  whether  a 
concavity  containing  it  requires  excavation,  or  whether  the  hyper- 
sensitive spots  are  not  to  be  excavated  after  treatment. 

Treatment  in  Cavities  of  Decay, — The  remedies  employed  in 
the  endeavor  to  reduce  or  abolish  hypersensitivity  in  a  cavity  of 

Dental  Cosmos.,  1901.  2  Ibid.,  1909,  p.  844. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS      401 

decay  at  the  time  of  operation  are  quite  numerous ;  few  are,  however, 
always  effective.    They  may  be  classed  under  two  headings : 

1 .  Those  which  temporarily  benumb  or  anesthetize  the  fibrillse  and 
prevent  the  transmission  of  sensation. 

2.  Those  which  chemically  destroy  the  fibrillse  for  a  distance,  thus 
preventing  transmission  of  sensation. 

Remedies  which  Benumb  the  Fibrill^e. — Chief  among  tnese 
for  its  universality  of  application  is  dryness.  Dentin,  which  protests 
against  even  the  touch  of  an  instrument  while  wet,  has  its  sensitivity 
so  lessened  after  the  application  of  a  rubber  dam  and  drying,  that  it 
may  be  cut  freely,  in  many  cases  without  the  aid  of  medicinal  agents. 
So  well  is  this  recognized  that  isolation  and  drying  of  teeth  are 
regarded  as  a  necessary  preliminary  to  cavity  preparation.  The 
degree  of  insensitivity  induced  is  in  proportion  to  the  dryness.  The 
drying  temporarily  deprives  the  dentinal  protoplasm  of  a  portion  of 
its  water,  and  inhibits  the  transmission  of  sensation  by  reducing 
functional  activity. 

A  continuous  but  gentle  blast  of  air,  passed  from  a  compressed-air 
apparatus  or  double  bulb  through  a  heated  metal  bulb  and  nozzle, 
or  through  an  electrically  heated  coil,  should  be  employed  until  the 
dentin  is  desiccated.  This  is  evidenced  by  its  extreme  whiteness. 
Other  forms  of  hot-air  syringes  may  be  substituted  with  less  satis- 
faction and  greater  fatigue  to  the  operator.  The  double  bulb  may 
be  operated  by  the  patient. 

The  application  of  absolute  alcohol  assists  the  drying  because  of 
its  affinity  for  water.  The  addition  of  a  little  menthol  to  the  alcohol 
assists  by  anesthetic  action.  The  pain  from  the  warm  air  may  at 
first  be  quite  severe,  but  even  in  greatly  hypersensitive  cases  the 
nozzle  of  the  syringe  may  soon  be  approximated  to  the  cavity,  though 
in  some  cases  it  may  be  necessary  to  make  an  application  of  a  mixture 
of  equal  parts  of  carbolic  acid  and  oil  of  cloves,  or  of  gum  camphor 
and  carbolic  acid  (phenol  camphor),  both  of  which  have  some 
anesthetic  effect.  Menthol  may  be  added  to  either.  When  desirable, 
their  effect  may  be  hastened  by  pressure  with  un vulcanized  rubber. 

An  instrument  known  as  the  "dehydrator"  causes  absolute  alcohol 
placed  in  a  special  chamber  between  the  bulb  of  the  hot-air  syringe 
and  the  nozzle  to  be  vaporized  upon  the  hypersensitive  dentin. 
The  drying  effect  is  thereby  augmented  and  the  dentin  satisfactorily 
obtunded. 

Some  degree  of  dryness  is,  as  a  rule,  a  necessary  preliminary  to 
success  with  other  applications. 

Following  dryness,  the  excavation  should  be  done  with  sharp 
instruments  and  burs.  The  latter  should  only  be  lightly  touched  to 
26 


402  DENTAL  CARIES 

the  dentin  and  be  revolved  at  high  speed.  Letting  the  bur  occa- 
sionally run  free  cools  it.  The  heat  of  friction  is  considerable  and 
highly  irritating. 

The  combination  of  potassium  carbonate  with  glycerin  makes  a 
water-extracting  combination  having  but  little  coagulating  power. 
For  this  reason  it  may  be  used  in  the  deeper  cavities,  but  not  in  cases 
of  almost  exposed  pulp,  as  in  such  cases  its  application  is  painful. 

I^ — Potassium  carbonate gr.  xv 

Glycerin fSJ 

Mix  in  a  mortar. 

To  be  applied  on  a  pellet  of  cotton.     (Flagg.) 

It  may  be  used  with  effect  even  upon  slightly  moist  dentin. 

Not  being  escharotic  to  the  gum,  this  remedy  is  exceedingly  useful 
about  the  sensitive  but  undecayed  necks  of  teeth,  and  may  be  freely 
applied  after  moderate  drying  of  the  parts. 

If  necessary,  the  patient  may  be  given  the  prescription  and  directed 
to  apply  by  means  of  a  clean  tooth-pick,  which  should  not  be  used 
a  second  time,  as  the  mixture  may  be  infected  and  spoiled. 

Its  pain  simulates  that  of  zinc  chlorid,  but  is  less  severe  in  its 
character. 

A  mixture  of  tannin  and  glycerin  has  a  similar  effect. 

I^ — Tannin 3J  or  5i.i 

Glycerin fgj 

Mix  in  a  warm  mortar. 

Refrigeration  by  a  spray  of  ether  or  ethyl  or  methyl  chlorid  reduces 
the  temperature  of  the  fibrils  and  pulp,  benumbing  them.  The 
rubber  dam  should  be  applied  to  isolate  the  teeth  operated  upon. 
Ether  is  applied  by  means  of  a  double-bulbed  atomizer,  or  one 
operated  by  compressed  air;  the  chlorids  are  contained  in  glass 
tubes  conveniently  capped.  The  cap  being  raised,  the  heat  of  the 
hand  causes  vaporization  of  the  agent  within  the  tube,  which  forces 
the  liquid  out  of  the  orifice  of  the  tube  in  a  fine  but  forcible  stream. 
A  spraying  nozzle  is  also  obtainable.  The  cavity  should  at  first 
contain  a  pellet  of  cotton,  in  order  that  the  dentin  may  be  gradually 
obtunded  and  painful  response  on  the  part  of  the  pulp  avoided.  The 
method  may  be  painful  in  application,  but  often  satisfactory.  Ether 
odorizes  the  operating  room,  and  a  flame  must  be  avoided. 

"Vapocain"  and  "potassocain,"  proprietary  agents  which  consist 
of  a  15  per  cent,  solution  of  cocain  in  ether,  are  applied  to  hyper- 
sensitive dentin  upon  the  theory  that  the  ether  enters  the  tubules, 
carrying  the  cocain  into  contact  with  the  fibrils;  the  ether  evapo- 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     403 

rates,  leaving  the  cocain  in  aqueous  solution  to  benumb  them.  This 
requires  several  minutes.  They  are  useful  in  the  deeper  cavities. 
Jack  recommends  that  the  cavity  acidity  be  neutralized  before  their 
application.^ 

Fig.  373 


Ethyl  chlorid  spray  tube. 


A  10  to  25  per  cent,  solution  of  cocain  hydrochlorate,  or  novocain 
in  water  may  be  forced  into  the  tubules  by  applying  it  on  a  pellet  of 
amadou,  placing  over  this  soft  vulcanite  rubber,  and  producing 
pressure  with  a  burnisher  for  from  three  to  six  minutes.  The  pressure 
should  be  gradually  applied.  A  gratifying  degree  of  dentinal  anes- 
thesia may  often  be  obtained. 

Adrenalin  chlorid  solution,  1  to  1000,  plus  chloreton^  or  cocain, 
has  been  used  in  this  manner  with  some  effect.  A  few  crystals  of 
the  cocain  or  novocain  may  be  picked  up  on  a  pellet  of  cotton  moist- 
ened with  warm  water  and  pressed  upon  the  cavity  surface. 

Miller^  has  shown  that  by  taking  a  modelling  composition  impres- 
sion of  the  cavity,  then  applying  a  few  threads  of  cotton  saturated 
with  cocain  to  the  floor  of  the  cavity,  then  placing  a  thickness  of 
rubber  dam  over  the  entire  cavity  surface,  replacing  the  modelling 
composition,  and  producing  pressure,  anesthesia  can  be  produced 
when  there  is  not  a  greasy  condition  of  the  cavity,  nor  thick  layers  of 
decalcified  dentin  nor  much  secondary  dentin  present. 

Cataphoresis  (Greek  kata,  down,  and  phoreo,  I  bear  or  bring)  is, 
in  technical  parlance,  the  transference  of  substances  from  the  anodal 
or  positive  pole  of  a  battery  toward  the  cathodal  or  negative  pole. 
They  are  thus  carried  into  the  tissues. 

Cataphoresis  is  to  be  distinguished  from  electrolysis,  by  which 
substances  are  decomposed  and  their  elements  carried  from  positive 
to  negative  or  from  negative  to  positive  poles,  according  to  their 
polarity.  In  cataphoresis  a  substance  is  carried  unchanged  from  the 
positive  toward  the  negative  pole,  after  the  manner  of  granules  in 
protoplasm  acted  upon  by  the  same  force.     (See  p.  20.) 


1  American  Text-book  of  Operative  Dentistry. 

2  Parke,  Davis  &  Co. 


3  Dental  Review,  1906. 


404  DENTAL  CARIES 

As  applied  to  dentistry,  a  primary  current  from  a  battery  arranged 
with  the  cells  in  series  has  the  positive  pole  or  conductor  connected 
with  a  resistance  or  current  controller,  capable  of  being  so  manipulated 
as  to  gradually  reduce  the  resistance  to  the  current  a  fraction  of  a 
volt  at  a  time.  This  is  called  a  "fractional  volt  selector."  This  is 
usually  a  broken  ring  of  graphite,  to  one  end  of  which  the  incoming 
current  is  admitted  by  means  of  the  conducting  cord  and  travelling 
indicator  (from  the  positive  or  carbon  pole  of  the  battery);  at  the 
other  end  the  current  passes  out  by  a  similar  cord,  which  in  turn 
is  -  attached  to  a  milliamperemeter,  or  instrument  recording  the 
quantity  of  current  passing  through  the  circuit.  From  this  a  cord 
leads  to  the  positive  electrode  applied  to  the  tooth  cavity.  To 
the  face,  neck,  or  wrist  of  the  patient  a  moist  electrode  (negative) 
is  applied,  which  by  its  conducting  cord  leads  the  current  back  to 
the  negative  or  zinc  pole  of  the  battery.  The  current  passes  through 
the  patient. 

The  milliamperemeter  is  a  convenient  but  not  an  essential  feature 
of  the  apparatus,  and  as  a  volt-selector,  a  rod  of  graphite  or  a  glass 
tube  with  water  resistance  may  be  used.  Fig.  374  shows  the  more 
elegant  apparatus  arranged  almost  as  described. 

In  the  use  of  the  cataphoric  apparatus,  the  tooth  is  securely  in- 
sulated by  well-ligated  rubber  dam  and  cotton  saturated  with  a 
solution  of  cocain  hydrochlorate  or  citrate,  of  a  strength  of  from  10 
per  cent,  to  a  saturated  solution  is  placed  in  the  cavity.  The  platinum 
anode  is  wrapped  with  cotton,  dipped  in  the  solution,  and  inserted 
into  contact  with  the  cotton  in  the  cavity.  The  controller  is  now  so 
manipulated  as  to  gradually  cut  out  its  resistance  to  the  current,  and 
the  high  resistance  of  the  dentin  is  gradually  overcome. 

The  cocain  solution  should  be  renewed  as  dryness  occurs,  as  dryness 
increases  the  resistance.  The  cocain  is  carried  along  the  fibrils  to 
the  pulp  by  the  electric  current,  and  dentinal,  followed  by  pulpal 
anesthesia  results. 

From  eight  to  fifteen  minutes,  or  sometimes  longer,  are  required 
for  dentinal  anesthesia,  which  loss  of  time  is  largely  regained  in  the 
facility  of  operation.^ 

Price^  has  shown  that  pulp  anesthesia  is  gained  more  readily  by 
concentrating  the  action  of  the  cocain  upon  the  pulpal  wall  by  means 
of  a  small  electrode.  If  general  dentinal  anesthesia  is  required  he 
prefers  this  method,  as  the  pain  receptivity  of  the  pulp  is  abolished. 
A  broader  application  anesthetizes  the  dentin. 

Woodward^  has  shown  that  in  the  latter  case  the  dentin  in  a  cavity 

1  Jack:  American  Text-book  of  Operative  Dentistry.    2  Dental  Summary,  April,  1903. 
3  International  Dental  Journal,  November,  1902. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     405 

upon  the  opposite  side  of  a  tooth  being  operated  upon,  may  remain 
sensitive. 

Fig.  374 


S.  S.  White  cataphoric  outfit. 

The  pulp  may  be  anesthetized  by  this  method  for  removal.     In 
difficult  conditions  this  is  a  very  valuable  means  of  therapeutics. 


406  DENTAL  CARIES 

The  pulp  is  not  injuriously  affected  in  ordinary  applications,  unless 
saturated  by  long  application.  A  reaction  resulting  in  hyperemia  may 
take  place.  To  obviate  this,  the  pulp  should  not  be  oversaturated,  the 
fibrils  should  be  treated  with  carbolic  acid,  and  in  deep  cavities  a 
non-conductor  should  be  used  before  filling. 

In  case  absolute  insensitivity  is  produced,  the  anatomy  of  the  pulp 
must  carefully  be  considered,  so  that  it  be  not  exposed  during  the 
excavation  of  the  cavity.  This  can  be  determined  by  instrumental 
examination.  Insulation  of  the  pulp  from  thermal  shock  subsequent 
to  filling  is  also  to  have  consideration. 

The  pulp  may  have  cocain  or  novocain  forced  into  it  by  means  of 
a  powerful  compound-pressure  syringe.  The  Meyers  syringe  is  one 
of  the  best.  It  is  filled  with  a  2  to  4  per  cent,  solution  of  cocain  or 
novocain  in  water;  a  convenient  drill  pit  is  made  with  a  No.  ^  bur; 
the  nozzle  of  the  filled  syringe  freed  of  air  is  forced  into  the  opening 
and  continuous  or  intermittent  pressure  produced  without  releasing 

Fig.  375 


The  Meyers  compound  syringe  for  forcing  cocain  solutions  through  the  dentinal 

tubules. 

the  point  for  several  minutes.  It  is  well  to  allow  the  air  to  escape 
from  the  pit  by  holding  loosely  for  a  moment.  No  general  cavity 
anesthesia  will  result  until  the  solution  has  infiltrated  the  area  of 
pulp  underlying  the  fibrillar  connections  with  the  pulp.  The  forcing 
of  cocain  into  so  delicate  a  tissue  should  stop  at  that  point,  as  more 
may  produce  expansive  pressure,  and  may  cause  a  later  pulp  reaction, 
as  cocain  is,  to  a  degree,  a  protoplasmic  poison.  The  method  is  useful 
in  pulp  extirpation  rather  than  in  hypersensitivity,  but  has  occasional 
use,  especially  in  cervical  cavities.  Secondary  dentin  is  difficult  of 
penetration,  and  gradual  approaches  must  be  made.  It  should  be  so 
injected  into  only  sound  dentin.  If  the  cervix  of  a  cavity  is  used  as 
the  point  of  injection,  the  pit  should  be  made  deeper  than  the  syringe 
nozzle  penetrates,  as  in  this  way  the  lateral  tubules  can  carry  the 
cocain,  otherwise  they  may  be  occluded  by  the  syringe  point.  The 
syringe  nozzle  may  be  made  flat  ended  and  the  pit  in  the  dentin  be 
made  with  a  cone-shaped  bur. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS      407 

Mucous  AND  Conductive  Anesthesia. — The  anesthetization 
of  the  branch  of  the  fifth  nerve  leading  from  the  tooth,  renders  it 
incapable  of  transmitting  sensation  to  the  brain.  In  principle  its 
application  does  not  differ  from  local  application  to  fibrils  or  pulp. 
The  nerve  paralysis  is  produced  nearer  the  brain,  as  it  were.  Novo- 
cain is  at  present  largely  substituted  for  cocain  for  this  purpose. 

Guido  Fischer  recommends  the  following  as  an  isotonic  solvent: 

Calcium  chlorid 0.04  gram. 

Potassium  chlorid 0.02  gram. 

Sodium  chlorid 0.05  gram. 

Distilled  water  (sterile) 100 .  00  grams  or  c.c. 

Add  novocain  1.0  or  1.5  or  2.0  grams,  to  make  a  1  to  2  per  cent, 
solution  as  desired.  At  the  time  of  use  add  two  drops  of  a  1  to  1000 
solution  of  synthetic  suprarenin  to  each  30  minims  of  solution — 
boil  for  sterilization.  When  only  occasionally  used,  a  sterile  tablet 
(ready  made),  containing  ^  grain  of  novocain  and  a  suitable  pro- 
portion of  synthetic  suprarenin,  may  be  dissolved  in  30  minims  of 
the  isotonic  solvent  or  normal  salt  solution,  and  the  whole  boiled  for 
sterility.  A  tablet  (E)  is  made  by  the  Farbwerke-Hoechst  Company 
and  consists  of: 

IJ — Novocain 0.02  gram. 

Suprarenin 0.00005  gram. 

Dissolve  in  30  minims  of  solvent  for  a  1  per  cent,  solution  and  boil. 

When  mucous  anesthesia  is  employed,  the  solution  is  injected  into 
and  beneath  the  periosteum,  both  buccally  and  lingually,  as  nearly 
over  the  apex  of  the  root  as  possible.  About  ten  minutes  are  required 
to  produce  satisfactory  pulp  anesthesia.  Fischer^  emphasizes  the 
following  conditions  for  success  in  mucous  anesthesia: 

1.  The  application  of  a  stasis  bandage  slightly  compressing  the 
carotid  artery  and  the  veins  of  the  neck,  to  help  retain  the  anesthetic, 
and  prevent  cerebral  anemia. 

2.  The  periosteum,  not  the  submucous  tissue  must  be  infiltrated. 

3.  One  injection  to  be  made  on  each  side  of  the  teeth.  The  fewer 
injections  the  better  the  effect. 

4.  The  part  must  be  sterilized  with  tincture  of  iodin  and  the 
sterile  needle  must  have  its  orifice  faced  toward  the  bone. 

5.  Slow,  moderately  strong  pressure  during  the  injection. 

6.  The  point  of  injection  must  be  compressed  with  the  finger, 
after  the  needle  is  withdrawn  to  allow  diffusion  of  the  anesthetic. 

'  Local  Anesthesia  in  Dentistry. 


408  DENTAL  CARIES 

In  conductive  anesthesia,  the  anesthetic  is  injected  into  the  tissue 
contiguous  to  a  nerve  trunk.  Its  infiltration  causes  anesthesia  of 
the  part  it  supphes.  Fischer  directs  that  for  upper  posterior  teeth 
supplied  by  the  posterior  superior  dental  branch  of  the  superior 
maxillary  division  of  the  fifth  nerve,  a  long  needle  should  be  driven 
into  the  mucosa  beneath  the  zygomatic  process  and  then  advanced 
upward  and  backward  to  the  foramen  at  which  the  nerve  enters  the 
tuberosity  of  the  maxilla.  One  c.c.  of  solution  is  introduced.  Pala- 
tally  a  mucous  injection  is  made  at  the  posterior  palatine  foramen. 
For  upper  first  molars  an  additional  palatal  mucous  injection  over 
the  first  molar  is  advised.  Ten  minutes  is  allowed  for  operative 
anesthesia.  The  upper  teeth  anterior  to  the  molars  being  supplied 
by  the  infraorbital  terminals  their  sensibility,  may  be  blocked  by 
conductive  anesthesia  of  the  nerve  within  the  infraorbital  foramen 
above  the  first  bicuspid.     A  1  per  cent,  solution  is  used. 

Fischer  directs  the  introduction  of  the  needle  into  the  reflection 
of  the  mucous  membrane  just  back  of  the  cuspid  apex  and  to  be 
advanced  upward  and  backward  to  the  location  of  the  infraorbital 
foramen,  when  some  force  is  required  to  force  the  anesthetic  into  the 
foramen.  Palatally  a  mucous  injection  is  made  parallel  to  the  axis 
of  the  roots  of  the  teeth  to  be  anesthetized. 

For  anterior  anesthesia  in  the  mandible,  injection  is  made  into  the 
region  of  the  mental  foramen,  and  as  well  a  lingual  mucous  anesthesia 
is  done.  For  complete  anesthesia  of  the  side  of  the  mandible,  injection 
is  made  in  the  soft  tissue  just  above  the  retromolar  triangle  in  the 
inside  of  the  ramus.  Twenty  minutes  are  allowed  for  complete  anes- 
thesia. The  technique  of  these  injections  and  the  local  anatomy  are  so 
beautifully  illustrated  and  described  in  Guido  Fischer's  book  on  Local 
Anesthesia  in  Dentistry  that  the  reader  is  urged  to  master  its  details 
from  a  work  devoted  exhaustively  to  the  subject.^ 

DiPLCEic  Anesthesia. — For  deep  anesthesia  about  a  molar,  the 
gum  may  be  anesthetized  and  a  cut  made  to  the  bone,  a  small  sterile 
drill  is  then  driven  through  to  the  cancellated  structure.  A  further 
injection  is  then  made  with  a  blunt  needle,  such  as  is  used  in  high 
pressure  work.  This  operation  has  been  modified  by  the  use  of  a 
needle  constructed  to  simply  indent  the  cortical  layer  of  bone,  so 
that  the  force  of  the  plunger  may  cause  the  direct  infiltration  of  the 
apical  tissue.  This  uses  the  principle  of  high  pressure  anesthesia 
as  applied  to  dentin. 

While  the  operation  of  diploeic  anesthesia  seems  heroic,  there  is 
no  good  reason  for  so  regarding  either  this  or  the  operation  of  conduc- 

Theodor  Blum  has  an  excellent  article  in  Items  of  Interest,  for  July,  1914.     ' 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     409 

tive  anesthesia  in  general  as  more  dangerous  than  ordinary  mucous 
injection.  The  rule  of  safety  lies  in  knowledge  of  anatomy,  safe 
dosage,  and  sterility — in  short,  in  correct  technique. 

The  introduction  of  a  5  or  10  per  cent,  solution  of  cocain  upon 
cotton  into  the  nostril,  upon  the  side  of  operation,  is  endorsed  by 
Peck,  of  Chicago,  as  a  means  of  anesthetizing  the  nerve  trunk 
leading  from  the  upper  incisors.  Escat,^  of  Toulouse,  France,  has 
observed  that  a  0.1  per  cent,  solution  on  cotton  about  the  size  of  an 
almond,  placed  in  the  nostril  in  close  proximity  to  the  anterior  edge 
of  the  inferior  turbinate,  will  in  twenty  minutes  anesthetize  the 
anterior  superior  dental  branch  of  the  fifth  nerve,  which  lies  in  close 
proximity  to  the  nasal  mucous  membrane  at  this  point.  The  entire 
tissue  about  the  incisors  and  cuspids  of  the  side  is  anesthetized,  as 
is  sometimes  that  of  the  opposite  side  in  part. 

Reflex  Anesthesia. — Claims  are  made  by  Dr.  William  H. 
Fitzgerald,  M.D.,  that  pressure  with  a  metal  probe  tipped  with 
cotton  upon  certain  parts  of  the  mouth  and  fingers,  will  produce 
satisfactory  oral  anesthesia  and  even  of  more  distant  parts.  Cura- 
tive effects  in  certain  body  diseases  by  proper  manipulation  are 
claimed.     The  method  is  too  new  for  recommendation  here.^ 

Soderberg^  has  shown  that  painless  excavation  of  cavities  other- 
wise uncontrollable  may  be  effected  by  the  use  of  nervocidin,  an 
alkaloid  obtained  by  Dr.  D.  Dalma  from  the  East  Indian  plant 
gasu-hasu..  Twenty-four  hours  are  required  for  complete  dentinal 
anesthesia  without  pulp  anesthesia  unless  a  second  application  be 
made. 

The  primary  effect  of  nervocidin  being  irritating,  Soderberg  recom- 
mends the  additional  use  of  cocain,  both  being  mixed  with  zinc 
sulphate  cement. 

I^ — Gum  arable 3J 

Zinc  sulphate §ss 

Water fgj— M. 

Dissolve  the  zinc  sulphate  in  the  water,  add  the  gum  arabic,  stir;  let  stand  for 
twenty-four  hours  and  strain. 

I^ — Of  above  solution foij 

Nervocidin gr.  x 

Cocain  hydrochlorid gr.  x — M. 

To  a  portion  of  the  latter  solution  add  uncalcined  zinc  oxid  to 
make  a  cement,  which  is  placed  in  the  dried  cavity.    Uncalcined  zinc 

1  Theodor  Blum  has  an  excellent  article  in  Items  of  Interest,  1908,  p.  181. 

2  Paper  read  before  the  N.  J.  State  Dental  Society,  July,  1914.  See  Items  of 
Interest  to  be  published  later,  and  Hogan,  Items  of  Interest,  June,  1913. 

3  Dental  Cosmos,  August,  1903. 


410  DENTAL  CARIES 

oxid  added  to  the  first  formula  makes  zinc  sulphate  cement.  After 
excavation  the  acidity  of  the  nervocidin  should  be  neutralized. 
Buckley^  has  recommended : 

I^ — Mentholis gr.  xx 

Chloroformi fgss 

Etheris f3J— M. 

Sig. — Place  a  little  in  the  cavity  after  the  rubber  dam  is  adjusted. 

Hot  water  supplied  by  a  tube  leading  from  a  coil  heated  by 
electricity  and  attached  to  the  water  supply  pipe  of  the  fountain 
cuspidor  has  been  recommended  by  A.  F.  Merriman,  Jr.,  for  the 
obtunding  of  hypersensitive  dentin  in  cases  in  which  dryness  is  not 
readily  obtainable,  nor  immediately  or  subsequently  desirable. 

It  is  claimed  that  satisfactory  analgesia  is  obtained,  and  that  the 
mucous  membrane  of  the  mouth  is  not  unduly  uncomfortable,  even 
when  the  heat  is  objectionable  to  the  finger  of  the  operator.  The 
advantages  of  the  method  for  excavation  and  grinding  are  obvious 
and  most  useful,  particularly  for  trimming  live  teeth. 

Remedies  which  Chemically  Destroy  the  Fibrils  for  a 
Distance,  Preventing  Transmission  of  Sensation. — Agents 
which  chemically  destroy  the  dentinal  protoplasm  form  the  most 
extensive  group  of  dentinal  obtundents.  They  include  salts  of 
metals,  such  as  zinc  chlorid  and  silver  nitrate;  carbolic  acid  and  its 
derivatives,  and  like  bodies;  the  cresols,  etc.;  mineral  acids,  notably 
sulphuric,  chromic,  and  nitric;  organic  acids — trichloracetic  and  lactic 
acids— ^  (full  strength) ;  alkalies — sodium  and  potassium  hydrates  and 
carbonates. 

Zinc  chlorid,  silver  nitrate,  and  carbolic  acid  all  cause  coagulation 
of  the  fibrils  of  the  dentin.  The  mineral  and  organic  acids  chemic- 
ally decompose  both  protoplasm  and  the  calcified  tissues.  The 
concentrated  alkalies  chemically  destroy  protoplasm  and  bring 
about  its  quick  dissolution.  Like  all  active  chemical  substances,  the 
extent  of  their  action  depends  upon  the  freedom  with  which  they 
are  applied. 

The  application  of  any  of  these  agents,  as  a  rule,  causes  pain,  the 
degree  of  suffering  being  usually  in  proportion  to  the  depth  of  the 
cavity.  For  this  reason  the  more  powerful  agents,  like  zinc  chlorid 
and  nitric  acid,  are  to  be  confined  to  cavities  of  moderate  depth, 
while  carbolic  acid,  especially  in  combination  with  the  oil  of  cloves, 
may  be  used  in  the  deeper  ones. 

Fused  zinc  chlorid  is  used  in  its  deliquesced  form,  and  is  most 
active  when  some  of  the  salt  is  still  undissolved  in  the  bottle.     Its 

1  Dental  Cosmos,  August,  1907,  p.  328. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     411 

pain  in  suitable  cavities  is  a  full,  bearable  one,  gradually  increasing, 
sometimes  in  waves,  until  a  crisis  is  reached,  when  the  pain  gradually 
ceases.  It  has  a  double  action,  not  only  coagulating  protoplasm, 
but  combining  with  its  water,  owing  to  its  affinity  for  the  latter. 
On  account  of  this  property  its  action  may  be  limited  by  warm  water. 

An  undue  action  of  the  zinc  chlorid  is  indicated  by  a  throbbing 
pain;  this  indicates  that  the  pulp  has  been  irritated.  When,  as  occa- 
sionally occurs,  no  pain  is  produced,  no  obtundent  effect  is  obtained. 
If  this  occur  regularly  the  drug  is  oversaturated  with  water. 

Bogue  has  suggested  that  cocain  crystals  be  incorporated  with 
the  chlorid  of  zinc  as  a  means  of  alleviating  the  pain  incident  to  the 
application. 

Miller,  following  Hoffheinz,  advocated  the  use  of  equal  parts  of 
zinc  chlorid  and  chloroform. 

Buckley  modified  this  by  using  the  following: 

I^— Zinc  chlorid gr  xx 

Chloroform, 

Alcohol aa     f§  iv— M. 

Certain  moderately  deep  cavities  may  be  filled  with  oxychlorid  of 
zinc  cement,  the  free  zinc  chlorid  acting  as  an  obtundent.  This 
requires  a  prolonged  action,  and  is  only  resorted  to  in  cases  which 
do  not  admit  of  immediate  work,  or  in  which  procrastination  is 
desirable. 

A  formula  of  wide  renown  is  known  as  Robinson's  remedy;  this 
may  be  made  in  one  of  two  ways: 

I^ — Potassium  hydrate 

(or  Sodium  hydrate) , 

Carbolic  acid P-  seQ-— M. 

Reduce  the  gelatinous  mass  formed  with  alcohol. 

Or, 

I^ — Sodium  hydrate  (deliquesced), 

Calvert's  crystal  carbolic  acid      ....     p.  seq. — M.     (Huey.) 
The  liquid  formed  is  spoiled  when  it  eflloresces  upon  the  sides  of  the  bottle  neck. 

The  painfully  caustic  action  of  the  sodium  or  potassium  hydrate 
is  modified  by  the  carbolic  acid. 

The  application  of  Robinson's  remedy  is  useful  in  the  simpler 
cavities  and  about  the  undecayed  but  hypersensitive  necks  of  teeth 
and  on  occlusal  surfaces.     It  is  escharotic  to  the  gum. 

If  this  remedy  or  zinc  chlorid  be  required  about  the  periphery  of 
deep  cavities  the  plan  suggested  by  Jack,  of  varnishing  the  cavity 
floor  with  chloro-percha  as  an  impenetrable  protective  is  valuable. 


412  DENTAL  CARIES 

A  method  similar  to  the  use  of  Robinson's  remedy  consists  in  apply- 
ing carbolic  acid  to  a  cavity  and  then  without  removing  it,  placing  a 
few  granules  of  sodium  dioxid.^  Sodium  dioxid  alone  in  a  slightly 
moist  cavity,  liberates  nascent  sodium  hydrate  (also  H2O2),  which 
will  destroy  the  gum  protoplasm,  and  is  somewhat  effective  in  hyper- 
sensitive dentin. 

Carbolic  acid  in  concentrated  form  may  be  applied  to  any  cavity. 
Jenkins,  of  Dresden,  has  recommended  that  it  be  used  hot;  it  is 
particularly  useful  for  cavities  containing  masses  of  softened  dentin. 
A  variation  consists  in  the  application  to  the  cavity,  upon  a  pellet 
of  cotton,  and  heating  it  with  a  hot  burnisher. 

Sodium  bicarbonate  is  at  times  an  efficacious  remedy,  and  may  be 
freely  applied  to  the  moist  cavity.  A  20  per  cent,  solution  of  am- 
monium carbonate,  applied  for  five  minutes  or  longer,  is  useful.^ 

The  nitrate  of  silver  powerfully  coagulates  fibrillar  protoplasm, 
forming  the  albuminate  of  silver,  which  turns  black  upon  exposure 
to  the  light.  It  is  useful  in  posterior  teeth  well  out  of  view,  and  to 
which  the  rubber  dam  cannot  well  be  applied.  It  is  also  useful 
about  undecayed  hypersensitive  necks  of  molar  teeth.  It  penetrates 
the  dentin  for  a  short  distance.  For  this  reason  its  use  is  ordin- 
arily confined  to  posterior  teeth,  though  in  some  obstinate  cases  of 
hypersensitive  necks  of  lower  incisors  and  cuspids  it  may  be  used. 
To  prevent  the  production  of  hypersensitivity  in  teeth  ground  for 
bridge-work,  it  should  be  applied  over  the  entire  crown.  It  may  be 
used  in  saturated  aqueous  solution  upon  the  dried  dentin,  or  the 
crystal  rubbed  upon  the  slightly  moistened  dentin.  The  crystal  or 
fused  silver  nitrate  rubbed  upon  abraded  and  sensitive  occlusal 
surfaces  often  affords  much  comfort. 

Craven's  method  consists  of  taking  up  a  few  crystals  upon  a  hot 
platinum  wire,  and  then  fusing  them  into  a  button  upon  its  rough- 
ened end.    This  is  then  rubbed  upon  the  dentin. 

Miller  has  shown  that  the  silver  deposit  lessens  the  penetration  of 
acid  decalcification  (Fig.  376) . 

The  subsequent  use  of  sodium  chlorid  assists  in  partially  removing 
the  stains,  argentic  chlorid  being  formed. 

Register  has  suggested  the  use  of  iodin  followed  by  ammonia  for 
this  purpose. 

Coming  into  contact  with  an  amalgam  filling,  or  a  bit  of  amalgam, 
an  intensely  black  deposit  is  instantly  produced,  which,  while  acid  at 
first,  is  useful  in  slowly  obtunding  dentin  in  cavities  out  of  view. 
Curiously  enough,  not  all  amalgams  do  this. 

1  H.  J.  Moore:  Dental  Review,  1906.         ^  Thiesing:  Dental  Cosmos,  Nov.,  1903. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     413 

For  severe  cases  not  yielding  to  local  treatment  at  the  time  desired, 
the  following  has  been  recommended.^ 

I^ — Trioxymethylene 

Orthoform p.  seq. 

Make  into  a  paste  with  carbolic    acid. 


Or, 


I^ — Menthol  crystals 5  parts. 

Phenol  crystals 4  parts. 

Reduce  to  a  syrupy  liquid  to  be  used  in  place  of  the  carbolic  acid  in  the  above 

formula. 


This  paste  is  applied  to  the  cavity  walls  over  even  decayed 
dentin,  covered  with  a  pellet  of  cotton,  and  sealed  in  with  temporary 
stopping  or  cement  for  twenty-four  hours  only.  Formaldehyd  gas 
is  liberated  in  the  nascent  state  and  desensitizes  the  fibrils  by  harden- 


FiG.  376 


Dentin  treated  with  silver  nitrate  at  a  only;  the  entire  surface  subjected  to  acid 
action  shows  penetration  at  b.     (Miller.) 

ing  and  fixing  them  as  in  histological  specimens.  The  orthoform 
acts  as  an  anesthetic  during  the  action  of  formaldehyd.  This  prin- 
ciple has  been  used  in  cavities  with  the  ordinary  37  per  cent, 
formaldehyd  solution,  applied  by  the  pressure  method-,  and  is  useful 
about  the  hypersensitive  necks  of  teeth.  Buckley^  has  recently 
introduced  a  modification  in  a  paste  form  having  similar  action. 

I^ — Neothesin  (Lilly) 3^o  grain. 

Trioxymethelene ^3  grain. 

Thymol ^yo'  grain. 

Petroleum  base,  coloring  matter,  and  fibre. 

(The  figures  indicate  the  approximate  quantities  in  one  application.) 
S. — Apply  to  dry  dentin  and  cover  with  cement  for  twenty-four  to  forty- 
eight  hours. 

1  G.  Mahe,  M.D.,  Paris:  Dental  Cosmos,  1904. 

2  Items  of  Interest,  December,  1914. 


414  DENTAL  CARIES 

In  shallow  labial  cavities  it  is  to  be  applied  and  covered  with 
very  adhesive  cement. 

In  shallow  cavities  and  upon  abraded  surfaces,  nitric  and  chromic 
acid  accurately  applied  in  small  quantity  upon  a  gold  probe  is 
useful.    Any  softened  dentin  must  later  be  removed  and  filled. 

For  very  obstinate  cases  of  cervical  hypersensitivity,  Flagg  recom- 
mended the  use  of  the  electric  cautery,  the  spots  to  be  seared.  A 
very  hot  burnisher  may  occasionally  serve. 

Aside  from  the  treatment  of  hypersensitive  dentin,  at  the  time  of 
operation,  analgesics  may  be  introduced  for  their  power  of  gradu- 
ally lessening  the  hyperirritability  of  fibrillar  protoplasm.  If  cotton 
wedges  are  introduced,  antiseptic  analgesics,  particularly  oil  of 
cloves  (or  eugenol),  equal  parts  of  oil  of  cloves  and  carbolic  acid, 
and  phenol  camphor,  or  Fletcher's  carbolized  resin,  may  be  used  on 
the  cotton  with  advantage. 

A  partially  prepared  cavity  may  be  moistened  with  eucalyptol 
and  temporarily  filled  with  temporary  stopping  or  gutta-percha. 
This  affords  rest.  If  the  gutta-percha  leak,  the  cavity  will  be  more 
sensitive. 

A  temporary  filling  made  by  mixing  zinc  oxid  with  Fletcher's 
carbolized  resin  or  eugenol  to  a .  stiff  paste  will  endure  for  some 
time,  and  reduce  hypersensitivity.  It  is  also  useful  as  an  antiseptic 
sedative  test  filling. 

I^ — Carbolic  acid, 

Colophony aa       §j 

Chloroform fgss— M. 

(Fletcher.) 

The  use  of  chalk  applied  nightly  in  a  superficial  cavity,  as  at  the 
cervix,  is  useful  for  this  purpose. 

In  cases  in  which  devitalization  is  intended,  arsenic  may  be  used 
as  an  obtundent  to  effect  a  deeper  placing  of  another  portion  as  a 
devitalizing  agent;  twenty-four  to  forty-eight  hours  are  required  for 
this  purpose.  If  left  long  enough  it  will  devitalize  the  pulp  even 
through  a  large  mass  of  dentin. 

There  is  no  safety  in  short  applications  as  a  means  of  obtunding 
dentinal  hypersensitivity.  The  pulp  may  die  even  after  seeming 
excavation  of  all  affected  dentin. 

Ninety  per  cent,  of  cavities  may  be  comfortably  excavated  with 
sharp  instruments  by  the  aid  of  dryness  and  carbolic  acid  or  simple 
obtundents.  A  small  percentage  require  the  use  of  strong  caustics, 
etc.,  while  in  a  still  smaller  number  some  of  the  extreme  measures 
are  necessary,  though  nitrous  oxide  is  admissible  in  all  cases. 


HYPERSENSITIVE  DENTIN  AND  ITS  THERAPEUTICS     415 

During  seasons  in  which  acid  fruits  are  consumed,  much  hyper- 
sensitivity may  be  induced.  This  should  always  lead  to  examination 
for  cavities  of  decay,  but  such  may  not  exist  or  may  be  properly 
filled. 

For  hypersensitivity  about  undecayed  necks  of  teeth,  the  mouth 
should  be  kept  in  an  alkaline  condition  by  means  of  dilute  phenol 
sodique  or  sodium  bicarbonate,  or,  better,  by  the  use  of  more  lasting 
mild  alkalies,  such  as  chalk,  or  milk  of  magnesia,  or  a  combination 
of  the  two.  The  manufacturers  of  milk  of  magnesia  recommend  a 
series  of  oil  mixtures;  6  drops  of  any  mixture  to  be  shaken  up  with 
the  contents  of  the  original  bottle  as  a  flavor  to  remove  the  naturally 
raw  taste  of  the  preparation,  w^hich  is  disagreeable  to  some  persons.^ 
The  following  are  two  of  the  simplest. 

I^ — Oil  of  bitter  almond 1  part. 

Oil  of  anise 3  parts. 

Or, 

I^ — Oil  of  cinnamon 3  parts. 

Oil  of  wintergreen 4  parts. 

The  use  of  potassium  carbonate  in  glycerin  is  indicated  and  may 
be  given  to  the  patient  for  free  use. 

For  hypersensitive  incisal  edges  or  occlusal  surfaces,  Robinson's 
remedy  may  be  thus  dispensed  with  a  caution  as  to  its  caustic  nature. 

At  times  zinc  chlorid,  Robinson's  remedy,  and  silver  nitrate  or  the 
actual  or  electric  cautery  must  be  used  by  the  operator. 

In  a  number  of  the  localized  cases  fillings  may  be  subsequently 
required  unless  rigid  prophylaxis  be  practised.  Prophylaxis  may 
remove  the  superficial  desensitized  layer,  and  the  application  require 
renewal.  I  have  been  informed  that  a  case  of  general  hypersensiti- 
vity was  cured  by  the  lemon  juice  treatment  given  for  systemic  con- 
dition. The  idea  is  worthy  of  attention.  It  might  be  explained 
upon  the  principle  of  induced  alkalinity  of  salivary  secretion  as 
organic  acids  are  known  to  increase  the  alkalinity  of  the  urine. 

In  cavities  not  permitting  exact  excavation,  oxyphosphate  of 
copper  cement  left  for  a  considerable  time  will  often  reduce  exquisite 
sensitivity. 

The  use  of  potassium  sulphocyanate  internally  in  case  of  great 
general  dental  hypersensitivity  has  had  good  results  claimed  for  it, 
especially  in  pregnant  women.     (See  p.  361.) 

1  Items  of  Interest,  1905,  p.  977. 


CHAPTER  XIV. 
DENTAL  CARIES:  THERAPEUTICS  AND  PROPHYLAXIS. 

According  to  the  depth  of  invasion  and  variations  in  the  thera- 
peutics involved,  caries  may  be  divided  into  eight  stages,  as  follows: 

L  Superficial  caries,  or  that  stage  in  which  the  enamel  has  been 
partially  decalcified,  but  the  dentin  not  affected  (Fig.  338). 

2.  Simple  caries,  in  which  the  dentin  has  been  affected  slightly, 
in  such  manner  as  ordinarily  to  compel  the  formation  of  a  cavity 
and  its  filling  (Figs.  344  and  347). 

3.  Deep-seated  caries,  in  which  the  complete  excavation  of  the 
cavity  renders  pulp  injury  a  possibility,  but  the  pulp  is  not  very 
dangerously  approached  (Fig.  353). 

4.  Almost  exposed  pulp.  This  is  a  refinement  of  the  preceding 
stage,  in  which  pulp  exposure  becomes  imminent  during  excavation 
of  the  cavity  and  special  therapeutics  are  demanded  (Fig.  377). 

5.  Exposed  pulp,  in  which  the  actual  exposure  of  the  pulp  by 
decay  or  by  accident  or  intention  during  excavation  renders  its 
treatment  necessary,  or  in  which  disease  of  the  pulp  compels  canal 
treatment. 

6.  Perforation  by  caries,  in  which  after  pulp  death  secondary  caries 
of  iientin  and  cementum  has  caused  an  opening  into  the  pericemental 
tract  (an  extension  from  the  condition  in  Fig.  362).     (See  Fig.  378.) 

7.  Loss  of  crown  fey  caries. 

8.  Loss  of  root  by  caries. 

Each  of  these  stages  of  caries  requires  special  consideration  and  a 
therapeutics  adapted  to  each. 

THERAPEUTICS    OF   SUPERFICIAL   CARIES. 

About  cavity  margins,  beneath  green  stain,  etc.,  along  bucco- 
cervical  margins,  and  at  points  of  approximal  contact  of  teeth  may 
frequently  be  seen  areas  of  enamel  decalcification,  the  enamel  not 
being  entirely  penetrated  (Fig.  338). 

It  is  possible  at  times  to  remove  the  decalcified  portion  by  means 
of  carborundum  strips,  files,  or  disks.  If  the  surface  be  highly 
polished  by  means  of  pumice  and  chalk,  and  subsequent  prophyl- 
axis be  employed,  the  practice  may  be  endorsed  for  the  better  grades 
(416) 


THERAPEUTICS  OF  SIMPLE  CARIES  417 

of  teeth,  and  particularly  in  the  anterior  part  of  the  mouth.  As  a 
rule,  however,  the  attempt  to  remove  supposed  superficial  enamel 
caries  demonstrates  the  fact  that  the  enamel  is  deeply  affected,  and 
in  all  probability  the  dentin  as  well.  The  attempt  to  remove  such 
caries  upon  proximal  surfaces  by  files  and  stones  results  in  tooth 
deformity,  the  exposure  of  dentin  to  the  fluids  of  the  mouth,  and  the 
destruction  of  the  contact  points,  except,  perhaps,  when  in  the 
anterior  teeth  a  lingual  approach  is  made.  It  is  sometimes  proper  to 
remove  the  slight  superficial  caries  found  about  a  cavity,  either  prior 
to  excavation  in  order  to  determine  the  real  cavity  boundary,  or 
after  excavation  if  such  removal  would  give  an  even  better  tooth 
form,  and  lessen  a  recurrence  of  decay,  or,  in  some  cases,  after  filling 
when  both  filling  and  margin  are  reduced  together  to  a  proper 
form  and  integrity  of  enamel.  Some  judgment  is  required  in  such 
a  matter,  and  no  enamel  should  be  so  treated  if  any  doubt  exist  as 
to  its  future  integrity,  but  the  cavity  should  rather  be  extended  to 
include  the  doubtful  area. 

It  may  be  considered  a  safe  rule  to  examine,  by  means  of  the  electric 
mouth  lamp,  any  cases  of  suspected  superficial  caries  in  order  to 
determine  the  depth  of  enamel  invasion. 

The  large  majority  of  such  cases,  especially  in  the  poorer  grades 
of  teeth,  will  be  found  to  be  of  the  class  called  here  simple  caries. 

Upon  the  labial  or  buccal  surfaces  of  anterior  teeth  a  superficial 
decalcification  may  be  found.  Whether  (1)  this  shall  be  removed 
and  the  surface  polished,  or  (2)  be  left  for  the  patient  to  care  for 
by  exact  prophylaxis,  or  (3)  be  excavated  and  filled,  depends  upon 
the  location,  the  depth  of  penetration,  and  the  progress  of  the 
enamel  decalcification.  The  writer  has  carried  forward  for  a  long 
time  numerous  white  crescentic  markings  *by  prophylaxis  which 
removes  microbic  plaques  and  food  and  aborts  decalcification, 
though  not  removing  the  tissue  decalcified. 

In  posterior  teeth  staining  with  silver  nitrate  alone  or  by  touching 
later  with  amalgam  to  produce  a  rapid  deposit  of  silver,  grinding 
off  with  stones  and  then  touching  with  silver  nitrate,  or  filling  the 
actual  cavity  with  oxyphosphate  of  copper  and  staining  and  watch- 
ing the  remaining  decalcification,  have  all  given  good  results  when 
conjoined  with  improved  prophylaxis  by  the  patient.  Superficially 
decayed  cementum  may  be  removed  or  not  and  silver  nitrate  applied. 

THERAPEUTICS    OF   SIMPLE   CARIES. 

The  cases  cited  above  as  requiring  excavation  and  all  detectable 
cavities  of  very  limited  depth  may  be  classed  as  cases  of  simple 
caries.    The  teeth  should  be  wedged,  apart  if  this  be  needed  for  access, 

27 


418  DENTAL  CARIES 

all  decalcified  enamel  and  dentin  removed,  the  cavity  properly 
extended  and  shaped,  and,  as  a  rule,  a  metal  filling  inserted.  All 
fissures  about  a  cavity  should  be  freely  opened  to  their  extremities, 
and  made  a  part  of  the  general  cavity. 

The  extension  upon  approximal  surfaces  should  include  all  super- 
ficial decay  that  cannot  be  so  disked  off  as  to  bring  the  filling  margin 
into  the  embrasures. 

,  The  treatment  of  simple  approximal  cavities  is  a  difficult  question. 
Undoubtedly  extension  enhances  the  longevity  of  the  fillings.  At 
times,  however,  the  cavities  may  be  kept  purely  approximal  and  by 
the  use  of  gutta-percha,  silicate  cement  or  combination  of  amalgam 
and  cement  renewed  or  repaired  as  required,  the  case  can  be  con- 
trolled for  many  years.  This  may  be  advisable  in  anterior  teeth 
where  gold  may  be  objectionable  or  when  systemic  conditions  or 
uncontrollable  sensitivity  warrant  it.  In  the  main,  if  endurable, 
cavities  in  posterior  teeth  should  be  extended,  otherwise  the  renewal 
of  the  fillings  will  probably  in  time  be  necessary.  In  the  anterior 
teeth  esthetics  often  warrants  keeping  the  cavities  small.  The 
question  is  one  which  can  be  settled  after  consideration  of  all  the 
requirements.  Subsequent  prophylaxis  is  of  importance,  and  to  that 
end  all  fillings  should  be  made  as  smooth  and  perfect  as  possible.    . 

If  a  simple  cavity  prove  inordinately  sensitive,  the  more  powerful 
remedies  may  be  freely  used  to  reduce  the  hypersensitivity,  and  the 
cavity  should  be  treated  with  carbolic  acid  before  filling,  particularly 
when  gold  is  to  be  used  in  cervicolabial  cavities  of  incisors.  By  this 
means  the  subsequent  effect  of  thermal  changes  is  lessened. 

THERAPEUTICS    OF   DEEP-SEATED   CARIES. 

In  this  stage  of  caries  there  is  usually,  although  by  no  means  always, 
an  easily  discoverable  cavity  of  size  (Fig.  353).  After  the  removal 
of  ragged  and  overhanging  enamel  margins,  and  of  loose  debris  in 
the  cavity,  it  is  noted  that  the  response  to  thermal  impulse  is  painful 
and  prompt.  In  washing  such  cavities,  water  at  a  temperature  of 
about  100°  F.  should  always  be  used;  cold  or  very  hot  water  being 
only  employed  in  cavity  irrigation  to  test  the  promptitude  of  response 
upon  the  part  of  the  pulp.     It  is  better  to  do  this  habitually. 

In  treating  hypersensitivity  of  dentin  carbolic  acid  is  to  be  pre- 
ferred, the  mineral  acids  are  avoided,  and  if  strong  agents  like  zinc 
chlorid  or  Robinson's  remedy  are  used,  the  cavity  floor  is  to  be 
varnished  with  chloro-percha  or  "cavitine"  varnish,  which  are 
impermeable.  If  necessary  the  sedative  temporary  methods  may 
be  employed.     (See  p.  414.) 


THERAPEUTICS  OF  DEEP-SEATED  CARIES  419 

The  use  of  nervocidine  or  of  trixymethylene  are  most  applicable  if 
sittings  are  a  few  days  apart.  For  methods  of  deahng  with  hyper- 
sensitivity see  p.  393. 

Cocain  cataphoresis  is  regarded  as  admissible  in  all  stages  of  caries. 

The  removal  of  all  the  softened  dentin,  which  should  be  done  in 
these  cases,  forms  a  cavity  of  such  magnitude  that  proximity  to  the 
pulp  is  evident.  The  softening  has  proceeded  for  a  distance  beneath 
the  enamel,  so  that  when  all  softened  dentin  is  cut  away  from  beneath 
it  the  latter  tissue  may  overhang  the  general  cavity  unsupported. 
These  overhanging  walls  are  cut  away  until  the  region  of  strong 
enamel  is  reached,  and  then  it  may  be  that  the  walls  still  overhang 
the  general  cavity.  It  is  usually  not  necessary  nor  advisable  to 
remove  this  portion  of  enamel. 

At  the  completion  of  excavation  the  pulpal  wall  of  the  cavity  will 
be  in  fair  proximity  to  the  pulp.  A  blast  of  cool  air  from  a  chip 
syringe  may  produce  an  immediate  response  upon  the  part  of  the 
pulp,  vigorous  in  proportion  to  the  thinness  of  its  dentinal  covering 
and  its  irritability. 

In  many  cases  non-conducting  substances  are  required  as  inter- 
mediates between  the  pulpal  wall  and  the  metal  filling.  In  many 
other  cases  the  metal  filling  may  be  placed  directly  upon  the  dentin 
without  danger.  In  some  cases  a  simple  layer  of  non-conducting 
varnish,  such  as  "cavitine,"^  will  be  sufiicient.  In  others  zinc  phos- 
phate or  gutta-percha  must  be  added.  The  degree  of  the  response  to 
a  blast  of  cool  air  will  afford  a  guide  to  the  nature  of  the  intermediate 
required  if  any  be  deemed  necessary.  In  no  case  should  varnish  or 
gutta-percha  be  allowed  to  remain  in  the  portions  of  cavity  that 
support  the  covering  filling  material,  and  which  is  subjected  to  the 
force  of  mastication.  The  resilient  nature  of  such  substances  will 
cause  the  loosening  of  the  filling  and  probably  induce  mechanical 
or  infective  irritation  of  the  fibrils  and  through  them  of  the  pulp 
(Fig.  377). 

In  some  cases  the  undermined  state  of  the  enamel  wall  necessitates 
the  use  of  an  adhesive  zinc  phosphate  as  a  means  of  support  by 
replacing  the  lost  dentin,  and  in  such  the  pulpal  wall  may  be  covered 
and  so  protected  from  impact  as  well  as  from  thermal  changes. 

The  action  of  zinc  phosphate  upon  dentinal  fibrils  and  the  pulp 
being  a  matter  of  some  doubt,  it  is  better  that  the  pulpal  wall  be 
varnished  before  it  is  introduced.    The  varnish  not  only  acts  as  an 

1  Cavitine  is  a  solution  of  trinitrocellulose  in  subacetate  of  amyl.  Gum  sandarac  in 
alcohol,  gum  copal  in  ether,  or  Canada  balsam  or  gum  dammar  in  chloroform,  about 
30  to  60  grains  to  the  ounce  of  solvent  and  a  little  hydronaphthol  added,  makes  an 
antiseptic  cavity  varnish. 


420 


DENTAL  CARIES 


Fig.  377 


impervious  coating,  but  also  serves  as  an  additional  non-conductor. 
If  made  antiseptic  it  is  still  more  useful. 

After  the  cavity  is  prepared  it  is  sterilized  and  dried,  as  described 
in  the  next  stage  of  caries,  is  coated  with  varnish,  and  Harvard  zinc 
phosphate  plus  5  per  cent,  powdered  thymol 
mixed  stiff  is  packed  into  the  undercuts  and 
over  the  pulpal  wall,  and  approximately  formed. 
When  set  the  enamel  margins  are  freed  of 
cement  and  the  cement  is  excavated  to  the  form 
required.  In  some  cases  cement  can  only  be 
placed  over  the  pulpal  wall,  owing  to  lack  of 
room  for  both  cement  and  the  covering  filling. 
In  such  cases  the  combined  use  of  soft  cement 
and  gold,  or  soft  cement  and  amalgam,  is  useful. 
In  deep-seated  caries  the  extension  of  cavity 
margins  in  such  a  manner  as  to  prevent  re- 
currence of  decay  is  demanded.  Upon  approxi- 
mal  surfaces  the  ideal  conditions  are  an  extension 
of  buccal  and  lingual  margins  to  a  point  which 
will  permit  a  contoured  metal  filling  to  have 
its  corresponding  buccal  and  lingual  margins 
well  irrigated  by  the  action  of  the  tooth-brush 
and  food  in  mastication.  Often  a  slight  alter- 
ation of  tooth  form,  together  with  contouring 
of  fillings,  accomplishes  the  end  desired  without 
undue  cutting  of  tooth  structure.  Thus  the 
cervical  margin  may  be  slightly  reduced  with  strips  or  disks  to  assume 
an  absence  of  contact,  but  the  enamel  must  not  be  totally  removed. 
The  lingual  or  buccal  margin  may  be  treated  in  a  similar  manner. 

The  cervical  margin  of  the  cavity  and  filling  are  best  protected 
when  overlapped  by  healthy  gum  tissue,  and  if  the  gum  be  ap- 
proached, should  be  so  arranged.  The  cervical  margin  should  always 
be  extended  beyond  the  contact  point  in  such  cases,  whether  carried 
beneath  the  gum  or  not.  Incisal  margins  are  to  have  similar  con- 
sideration. 

Firm  approximal  contact  of  fillings  or  filling  and  tooth  are  required 
to  prevent  packing  of  food  into  the  interproximal  space.  This  would 
both  injure  the  gum  and  introduce  the  fermentable  element  in  caries 
production.  The  point  of  contact  should  be  neatly  rounded  to 
produce  a  normal  contact.  This  contact  should  be  obtained  even  if 
the  filling  must  be  overcontoured. 

An  exception  may  at  times  be  made  where  a  space  has  previously 
naturally  existed,  and  the  gum  margin  is  healthy. 


illustrat- 
ing the  use  of  pulp 
protectors:  V,      a 

layer  of  varnish;  GP, 
a  layer  of  low  heat 
gutta-percha,  or  in 
case  of  exposure  a 
layer  of  Jodoformagen, 
or  zinc  oxid  and  thy- 
mol in  which  case  the 
varnish  is  omitted ; 
ZP,  zinc  phosphate; 
with  or  without  thy- 
mol added;  M,  metal 
covering. 


THERAPEUTICS  OF  ALMOST  EXPOSED  PULP  421 

Teeth  should  never  be  joined  by  filhngs  alone,  as  one  or  both  will 
usually  loosen.  If  necessary  for  the  protection  of  the  gum,  both  may 
be  crowned  and  the  crowns  united  by  solder,  or  a  staple  may  be 
placed  in  the  pulp  canals  of  the  two  teeth.  About  this  a  common 
filling  may  be  built.  It  may  be  that  gold  inlays,  locked  in  spacious 
"doll  heads"  or  the  occlusal  surfaces  of  both  teeth,  and  extending 
over  to  distal  approximal  surfaces  as  well  as  into  the  cavities,  may  be 
joined  or  cast  double  as  a  means  of  support.  The  strain  upon  such 
fillings  is  very  great  when  occlusion  exists,  as  teeth  are  bodies  with 
individual  motion  and  are  apt  to  be  pushed  away  from  the  filling. 
(See  Pyorrhea  Alveolaris  and  Gingivitis.) 

THERAPEUTICS    OF   ALMOST   EXPOSED   PULP. 

In  this  stage  of  caries  complaint  is  usually  made  that  for  some 
time  pain  has  been  produced  by  the  presence  in  the  mouth  of  cool 
or  hot  substances.  Several  classes  of  almost  exposed  pulps  may  be 
discovered  after  opening  the  cavity  and  removing  the  bulk  of  the 
decayed  dentin.  In  the  simplest  class  the  pulpal  wall  may  be  found 
sound  after  removal  of  all  decalcified  dentin.  This  makes  practically 
a  case  of  deep-seated  caries,  and  is  to  be  treated  as  such,  the  close 
approach  to  the  pulp  simply  demanding  additional  precautions  as 
to  non-conduction,  prevention  of  compression,  and  infection.  The 
cavity  is  to  be  neutralized  with  a  solution  of  sodium  bicarbonate  or 
5  per  cent,  sodium  dioxid  solution,  etc.,  and  dried;  over  the  pulpal 
wall  "cavitin"  with  hydronaphthol  added  or  other  antiseptic  varnish, 
and  dried  again. 

I^ — Hydronaphthol gr.  ij 

Alcohol gtt.  XX — M. 

Add  to  the  half-ounce  bottle  of  "cavitine." 

A  thin  wafer  of  softened  gutta-percha  is  to  be  laid  over  the  pulpal 
wall  in  such  manner  as  not  to  interfere  with  the  introduction  of 
cement.  In  place  of  these  any  of  the  pulp  capping  cements  may  be 
used  as  a  first  layer  (Fig.  377).  Harvard  zinc  phosphate  mixed  to 
consistency  just  suited  to  the  case  may  be  pressed  laterally  into  the 
undercuts,  and  will  spread  nicely  over  the  gutta-percha  without 
pressure.  Under  no  circumstances  must  the  superstructures  depend 
upon  the  gutta-percha  base  as  a  support,  as  the  filling  may  loosen 
or  the  wall  be  broken. 

The  operation  may  be  varied  for  cases  of  but  limited  retaining 
periphery  by  gently  spreading  the  zinc  phosphate  over  the  varnish, 
or,  in  some  cases,  the  gold  and  zinc  phosphate  or  amalgam  and  zinc 
phosphate  combination  may  be  required. 


422  DENTAL  CARIES 

In  the  use  of  gold  and  zinc  phosphate  a  portion  of  crystal  gold  is 
gently  tapped  into  a  mass  of  soft,  quick-setting  cement  placed  over 
the  varnish  and  the  setting  of  the  cement  awaited.  The  gold  is  then 
condensed  and  more  added. 

With  the  amalgam  and  zinc  phosphate  combination,  after  placing 
the  gutta-percha,  soft  cement  is  placed  upon  one  cavity  margin, 
and  a  ball  of  previously  prepared  amalgam  is  laid  upon  it.  Pressure 
upon  the  amalgam  by  means  of  a  ball  burnisher  causes  the  cement  to 
be  spread  over  the  cavity  wall  in  advance  of  the  amalgam.  It  practi- 
cally inlays  the  metal  filling,  but  permits  a  better  marginal  joint  with 
the  metal.  The  margins  are  freed  of  amalgam  and  cement,  and  the 
operation  is  completed  with  amalgam.  It  also  prevents  the  shifting 
and  dislodgement  in  any  degree  of  the  metal  filling  which  sometimes 
occurs  in  the  act  of  introduction,  unless  guarded  against. 

This,  of  course,  refers  to  locations  in  which  the  latter  is  indicated. 
The  cement  in  the  combination  increases  the  adhesion  and  prevents 
leakage  and  the  discoloration  of  the  walls  by  the  amalgam.  A  trifle 
of  thymol  added  to  the  cement  (1  to  20)  imparts  to  it  an  antiseptic 
character  without  impairing  its  integrity  as  a  cement. 

The  second  class  of  almost  exposed  pulp  is  that  in  which  thorough 
excavation  would  cause  exposure  of  the  pulp. 

If  the  dentin  be  of  the  disintegrated,  boggy  sort,  it  should  be 
removed  regardless  of  exposure;  but  if  it  be  simply  softened  by 
decalcification  and  be  quite  firmly  adherent  to  the  cavity  floor,  and 
particuarly  if  it  be  somewhat  thickly  distributed,  the  deeper  layers 
may  be  left  in  situ,  as  a  pulp  covering. 

In  such  cases  all  lateral  walls  should  be  thoroughly  excavated  and 
only  a  thin  layer  left  over  the  pulp  horns.  While,  without  doubt,  the 
tubules  of  decalcified  dentin  are  liable  to  be  invaded  by  bacteria. 
Miller  has  shown  that  frequently  such  dentin  may  exist  without 
invasion,    (See  Fig.  356.) 

The  argument  that  such  dentin  contains  poisonous  products  of 
bacteria  deleterious  to  the  pulp  does  not  seem  borne  out  by  results 
in  carefully  handled  cases.    Decalcification  is  not  putrefaction. 

That  some  of  these  protected  pulps  may  die  is  a  fact  not  to  be 
disputed,  but  that  many  live  in  security  is  also  true.  Whether  such 
dentin  can  be  recalcified  has  not  yet  been  scientifically  shown,  but 
certain  cases  treated  with  oxychlorid  of  zinc  have  shown  evidences 
of  it,  and  Miller  records  cases  of  hardening  of  such  caries  even 
without  treatment. 

The  treatment  required  for  this  dentin  is:  (1)  Neutrahzation  of 
the  acid  present;  (2)  saturation  with  a  permanent  antiseptic;  (3)  an 
antiseptic  non-conductive  covering. 


THERAPEUTICS  OF  ALMOST  EXPOSED  PULP  423 

After  drying,  a  weak  solution  of  sodium  bicarbonate  or  ammonium 
carbonate  will  accomplish  the  first  requirements.  The  dentin  is  then 
thoroughly  dried  and  saturated  with  "cavitine"  varnish  contammg 
hydronaphthol,  or  a  solution  of  Canada  balsam  containing  hydro- 
naphthol,  or  thin  chloro-percha  containing  aristol  or  iodoform,  or 
the  formaldehvd  preparation  known  as  "  Jodof ormagen"  may  be 
spread  over  it',  or  oxychlorid  of  zinc,  the  fluid  of  which  has  been 
diluted  one-third  with  water,  may  be  used  as  a  covering  (use  fluid 
2  drops;  distilled  water,  1  drop),  or  a  mixture  of  zinc  oxid  and  thymol 
may  be  melted  over  it. 

Wifliamsi  suggests  that  the  decalcified  dentin  be  first  saturated 
with  absolute  alcohol  for  one  minute,  then  dried,  then  wet  with  oil 
of  cloves  for  one  minute,  then  again  dried,  after  which  the  varnish, 
etc.,  is  to  be  used.  Solution  of  sulphate  of  copper  may  be  used  to 
saturate  the  dentin,  after  which  it  should  be  dried  and  encased  in 
varnish,  etc.    This  last  only  in  posterior  teeth. 

The  use  of  these  preparations  obviates  the  necessity  of  sealing 
temporary  antiseptics  in  the  cavity,  as  they  are  in  themselves  more 
or  less  permanently  antiseptic.     The  rigid  preparations  are  most 
convenient.      Over    them    zinc    phosphate,    made    antiseptic    with 
thymol  (1  to  20),  is  packed  or  flowed,  and  if  any  doubt  exist,  the 
cavity  is  temporarily  sealed  with  gutta-percha  or  temporary  cement. 
When  all  doubt  is  at  rest  the  metal  filling  may  be  placed.    In  another 
method,  useful  in  doubtful  cases  in  determining  the  possible  bad 
reaction  of  the  pulp,  a  quite   stiffly    mixed   paste  of  eugenol  and 
Hubbuck's  zinc  oxid  may  be  introduced  into  the  base  of  the  cavity, 
gently  pressed  to  place  with  cotton,  and  covered  with  sandarac  on 
cotton,  or  at  a  subsequent  sitting  part  of  it  may  be  left  as  a  reason- 
ably firm  antiseptic  foundation.     If  desired,  the  entire  cavity  may 
be  filled  with  it,  or  better,  to  a  slightly  concave  surface.    Exposed 
to  the  saliva  it  hardens  to  a  degree  sufficient  to  act  as  a  cement 
temporary  filling  for  weeks  or  months,  or,  occasionally,  even  years.^ 
In  some  cases  of  deep-seated  caries  in  which  gold  filling  is  desirable, 
but  in  which  linings  are  contra-indicated,  yet  in  which  immediate 
.filling  with  metal  would  involve  such  thorough  excavation  as  to 
endanger  pulp  vitality  either  as  the  result  of  excavation  or  subsequent 
thermal  shocks,  oxychlorid  of  zinc  may  be  placed  in  the  peripherafly 
prepared  cavities,  and  over  considerable  masses  of  decalcified  dentin 
If  allowed  to  remain  for  several  months  (three  to  six)  the  oxychlorid 
stimulates  the  pulp  to  the  formation  of  some  secondary  dentin,  and 
complete  excavation  to  a  sound  basis  may  be  made.    There  is  also 

1  Items  of  Interest,  1898.  '  Dr.  S.  Blair  Luckie. 


424  DENTAL  CARIES 

some  evidence  of  hardening  of  the  dentin.  This  method  is  open  to 
the  possible  objection  that  secondary  dentin  is  a  source  of  future 
trouble,  but  the  method  has  its  advantages  in  badly  decayed  anterior 
teeth.^  In  very  deep  cavities  the  fluid  of  the  oxychlorid  should  be 
diluted  one-third  with  distilled  water  for  the  first  portion. 

In  these  cases  porcelain  inlays,  with  their  underlying  cement, 
should  have  due  consideration  as  therapeutic  means. 

In  deep  and  very  deep-seated  caries,  in  situations  in  which  dis- 
coloration is  not  of  great  moment.  Jodoformagen  may  be  placed 
over  the  pulpal  wall,  avoiding  the  bearings  and  the  cavity  filled  with 
oxyphosphate  of  copper  for  its  antiseptic  value.  The  cavity  may  be 
entirely  filled  with  it,  or  it  may  be  used  as  a  combination  with 
amalgam.  Copper  amalgam  alone  ordinarily  becomes  disintegrated 
and  caries  recurs.  Occasionally  it  lasts  well  (especially  Sullivan's) ; 
copper  and  its  salts  are  germicidal  in  a  short  time.  The  ordinarily 
good  behavior  of  somewhat  doubtful  dentin  under  it  is  thus  explained. 

Dobrzyniecki^  (Budapest),  in  eight  experimental  cases  upon 
microscopically  sound-looking  dentin,  claims  to  have  found  the 
Bacillus  gangrense  pulpee  vital  after  months  of  enclosure  under 
sealed  dressings  of  camphor,  concentrated  carbolic  acid,  or  eucalyp- 
tus oil.  All  other  organisms  were  devitalized.  As  Arkovy's^  experi- 
ments showed  the  decided  influence  of  carbolic  acid  over  this 
organism,  and  as  root-canal  antiseptics  are  nearly  always  successful 
in  cases  of  moist  gangrene  of  the  pulp  (Bacillus  gangrense  pulpse 
Arkovy),  the  difficulty  of  destroying  this  germ  by  germicides  left 
indefinitely  in  the  cavity  must  be  accepted  with  reservation. 

In  some  desperate  cases  with  the  walls  frail,  the  cements,  either 
zinc  phosphate  or  so-called  silicate  cements,  or  oxyphosphate  of 
copper  cements,  may  be  used  as  a  last  resort  before  crowning.  The 
silicate  cements  are  less  soluble  in  the  acids  contained  in  saliva  or 
formed  from  carbohydrates  against  the  filling  than  are  the  zinc 
phosphates. 

Hinkins  and  Acree*  claim  that  one-fifth  of  1  per  cent,  is  sufficient 
to  dissolve  the  zinc  phosphate,  and  that  enough  acid  elements  enter 
from  the  blood  to  affect  it. 

The  silicate  cements  dissolve  more  readily  under  friction  than 
under  the  action  of  acid,  so  that  of  two  fillings  the  one  which  is  not 

1  In  some  cases  of  this  sort  seen  by  the  writer,  and  observed  for  from  ten  to  twenty 
years,  the  ill-results  of  oxychlorid  of  zinc  claimed  have  not  been  observed.  In  one  case, 
after  sixteen  years,  a  lateral  incisor  crown  broke  off,  and  the  pulp  was  found  to  have 
receded,  but  was  otherwise  apparently  healthy.  The  question  is  one  of  the  advisability 
of  immediate  devitalization,  with  its  advantages  and  disadvantages  in  anterior  teeth, 
or  of  a  possible  remote  pulp  death,  etc. 

2  Soderberg  upon  Arkovy:  Dental  Cosmos,  1899.  '  Ibid. 
4  See  Dental  Cosmos,  June,  1901,  and  March,  1905. 


THERAPEUTICS  OF  EXPOSED  PULP  425 

exposed  to  attrition  or  brush  action  is  usually  in  better  condition 
after  about  two  years.  Much  care  is  necessary  to  prevent  the  dis- 
coloration of  silicate  cements. 

THERAPEUTICS    OF   EXPOSED   PULP. 

The  exposure  of  the  pulp  may  be  the  direct  result  of  caries;  the 
removal  of  boggy,  disintegrated  dentin  may  produce  it,  or  it  ma^' 
be  the  result  of '  the  removal  of  a  last  layer  of  decalcified  dentin 
or  of  the  careless  or  inadvertent  perforation  of  sound  dentin  by 
instruments.  Fracture  or  abrasion  are  occasionally  responsible  for 
exposure.    Erosion  rarely  causes  it. 

Diagnosis.— After  excavation  of  the  cavity,  washing  with  tepid 
water,  and  moderate  drying,  direct  vision  or  a  reflected  image  in  the 
mouth  mirror  may  reveal  the  area  of  exposure  as  a  round  opening 
occupied  by  a  pinkish  or  red  body.  If  the  exposure  be  reasonably 
large,  pulsation  of  the  red  body  may  usually  be  observed.  The 
exposure  may  be  so  slight  as  to  be  invisible,  the  depth  of  the  cavity, 
however,  indicating  that  exposure  probably  exists.  Bleeding  is  a 
certain  guide,  but  bleeding  from  the  gum  margin  must  be  borne  in 
mind.  Truman  advises  that  finely  carded  cotton  be  gently  passed 
over  the  cavity  walls,  exposure  being  detected  by  the  momentary 
pain  produced  when  the  fibres  pass  over  the  area  of  exposure. 

As  this  test  may  fail,  in  cases  of  known  exposure,  it  is  not  altogether 
reliable,  but  is  fairly  so  when  pain  is  produced,  though  hypersensitive 
dentin  must  be  borne  in  mind. 

A  finely  pointed  probe  may  be  gently  dragged  over  the  pulpal 
wall  and  catches  in  the  orifice  of  exposure,  however  small.  A  slight, 
quick  start  upon  the  part  of  the  patient  is  usually  elicited.  This  may 
consist  simply  of  a  winking  of  the  eyelid.  Flagg  warned  against 
requesting  an  affirmative  nod  by  the  patient,  as  this  would  cause 
injury  to  the  pulp.  Delicately  used,  this  test  is  the  most  reliable  in 
all  classes  of  cases,  and  is  not  painful. 

It  is  to  be  remembered  that  disease  may  have  caused  a  loss  of  a 
portion  of  a  pulp  horn,  in  which  case  the  cotton  test  will  fail;  gentle 
exploration  will  detect  the  amount  lost.  Blood,  or  pus  followed  by 
blood,  or  sensation  after  entering  the  horn  of  the  pulp  cavity,  are 
evidences  of  exposure. 

Excruciating  pain  following  mastication,  or  pressure  or  suction 
exerted  upon  the  cavity  by  means  of  the  tongue,  are  subjective  symp- 
toms indicating  a  probable  diagnosis  of  exposure.  Increase  of  pain, 
or  throbbing  pain  following  the  use  of  salt,  sweet,  or  acid  foods,  is 
fairly  indicative  of  a  practical  exposure. 


426  DENTAL  CARIES 

Treatment. — An  exposed  pulp  is  either  to  be  capped  or  removed 
and  the  canals  filled. 

The  consensus  of  opinion  is  that  ordinarily  all  pulps  should  be 
removed,  except  those  freshly  exposed  by  removal  of  simply  decal- 
cified dentin  and  by  accident.  There  is  no  certainty  that  pulps 
exposed  by  caries  or  practically  so  will  live  under  capping  materials, 
but  the  attempt  may  be  made  at  times  for  special  reasons. 

Freshly  exposed  pulps  may  be  capped  or  removed.  Perhaps  a  good 
rule  would  confine  capping  to  anterior  teeth  of  the  better  grades  in 
patients  in  good  physical  condition,  and  to  pulps  in  teeth  having 
incomplete  roots.  The  improved  methods  of  pulp  removal  and  canal 
antisepsis  warrant  pulp  destruction  as  a  safer  method  than  capping 
in  most  posterior  teeth.  Even  in  anterior  teeth  pulp  removal  for 
anchorage  purposes,  if  needed,  is  quite  warrantable.  The  advan- 
tages of  capping  are  maintenance  of  tooth  translucency  and  the 
avoidance  of  canal  work. 

The  disadvantages  are:  (1)  Possible  death  of  the  pulp  by  hyper- 
emia due  to  conduction  of  thermal  changes.  (2)  An  overproduction 
of  secondary  dentin,  the  production  of  pulp  nodules,  or  other  degen- 
erative changes,  the  pulp  becoming  exhausted  and  death  ensuing. 
Increased  difficulty  of  canal  treatment  may  result.  (3)  Disease  of 
the  pulp  due  to  infection  beneath  the  capping  material.  (4)  The 
time  required  for  assurance  of  success  or  failure. 

The  object  sought  in  capping  is  the  protection  of  the  pulp  from 
thermal  changes,  infection,  and  compression,  as  either  is  fatal  to  pulp 
vitality.  This  is  best  accomplished  by  placing  in  contact  with  the 
pulp  an  antiseptic  paste  beneath  a  metal  cap,  or  an  antiseptic 
cement  having,  when  set,  sufficient  rigidity  to  permit  .other  work 
to  be  done.  In  the  latter  case  the  capping  material  may  be  spread 
over  the  pulp  by  means  of  an  instrument  or  be  carried  on  oiled  paper 
which  may  be  stripped  off  after  the  cement  has  set. 

Prognosis  is  favorable  for  the  cases  selected  as  suggested. 

Pulp  Capping. — The  metal  cap  should  be  made  of  platinum  or  gold 
for  anterior  teeth.  Tin,  lead,  or  silver  may  be  used  posteriorly.  After 
punching  or  trimming  to  shape  it  should  be  made  concavo-convex 
by  pressing  it  into  soft  wood  by  means  of  the  rounded  end  of  an 
instrument  handle.  A  film  of  wax  is  placed  on  the  convex  side; 
a  warmed,  small  burnisher  is  attached,  and  the  cap  is  adjusted  in 
proper  position  by  trying  in  the  cavity.  It  is  then  to  be  filled  with 
the  capping  material  (a  little  of  the  latter  placed  in  any  depression 
at  the  point  of  exposure  in  order  to  exclude  air) ;  then  one  side  of  the 
cap  is  laid  upon  the  dentin  and  the  other  gradually  brought  down, 
and  the  edges  of  the  cap  firmly  adapted  to  the  dentin.    This  causes 


THERAPEUTICS  OF  EXPOSED  PULP  427 

the  paste  to  exude  from  beneath  the  cap.  Any  excess  is  gently 
removed  with  an  excavator  if  not  of  an  immediately  setting  paste. 
A  little  soft,  quick-setting,  zinc  phosphate  cement  plus  thymol  or 
oxychlorid  of  zinc  cement  is  now  run  over  the  floor  as  a  protection 
and  when  set  is  allowed  to  go  as  a  test.  Later  a  partial  excavation 
of  the  cement  is  done  and  better  zinc  phosphate  or  silicate  cement 
placed,  or  gutta-percha  used  as  a  further  test,  which  is  allowed  to 
remain  a  year. 

These  may  be  renewed  as  worn  out  if  desirable,  or  a  portion  of 
the  covering  filling  may  be  cut  away  and  metal  introduced.  In  all 
cases  capping  materials  are  not  to  be  allowed  to  support  the  super- 
jacent filling  materials  which  should  have  their  own  support  upon 
the  cavity  walls  as  shown  in  Fig.  377).  In  case  a  plastic  filling  is 
desirable  in  any  event,  the  operation  is  to  be  completed  at  the  time 
of  capping  or  at  a  subsequent  sitting. 

The  materials  used  with  success  as  pulp  cappers  are: 

1.  A  mixture  of  oil  of  cloves  and  zinc  oxid  (equal  parts  of  car- 
bolic acid  and  oil  of  cloves  may  be  used  as  the  menstruum).  Hub- 
buck's  zinc  oxid  or  cement  powder  may  be  used.  This  is  mixed  to  a 
consistency  which  will  flow,  yet  set  after  some  hours  or  days. 

2.  Oxysulphate  of  zinc,  the  fluid  of  which  is  a  saturated  solution 
of  zinc  sulphate  in  water.  The  powder  is  uncalcined  zinc  oxid.  This 
will  make  a  thin,  creamy  paste  which  flows  readily  and  sets  quickly. 
A  trifle  of  aristol,  iodoform,  or  hydronaphthol  may  be  added  to  any 
setting  cement. 

3.  Plaster  of  Paris  mixed  with  a  1  per  cent,  solution  of  formaldehyd 
in  water  will  make  an  antiseptic,  quick-setting  paste. 

4.  "  Jodoformagen."  This  substance  is  said  to  have  a  mixture  of 
eugenol  and  carbolic  acid  for  the  fluid,  while  the  powder  is  of  zinc 
oxid,  containing  paraform,  the  solid  form  of  formaldehyd.  It  also 
contains  salts  of  iodin.  A  cement  is  formed  which  sets  quickly, 
and  must,  therefore,  be  made  very  thin  when  placed  in  the  cap. 
This  material  has  been  successful  as  a  capper  even  in  exposures  by 
caries,  owing  to  its  intense  germicidal  power.  It  is  claimed  that 
the  formaldehyd  penetrates  the  tissue  of  the  pulp  for  a  distance, 
yet  permits  its  return  to  normality. 

5.  Oxychlorid  of  zinc,  with  the  fluid  diluted  with  50  per  cent,  of 
distilled  water  (1  to  2),  will  cap  successfully.  It  is  well  to  add  a  little 
powdered  thymol  to  lessen  irritation  and  add  antisepsis. 

6.  Crystallized  thymol  can  be  gently  melted  on  the  end  of  a 
burnisher  and  dropped  on  the  point  of  exposure  to  crystaUize,  or 
a  piece  of  a  mixture  of  thymol  and  zinc  oxid,  made  by  melting  the 
former  and  incorporating  the  latter,  may  be  added  to  the  drop  of 


428  DENTAL  CARIES 

thymol  in  position  and  melted  with  a  warm  burnisher.  Setting 
cappers  may  be  used  without  metal.  Of  these  capping  materials 
the  writer  prefers  jodoformagen,  which  though  proprietary,  has  posi- 
tive sedative  as  well  as  germicidal  and  persistent  antiseptic  value. 

Results  of  Capping. — If  pain  be  initiated  when  the  cap  is  placed 
and  recur  later,  compression  has  occurred,  and  the  capping  must  be 
removed,  the  pulp  quieted,  and  the  capping  renewed  or  the  pulp 
removed.  Though  no  sensation  be  produced  at  the  time  of  operation, 
a  reaction  to  thermal  changes  may  occur.  If  this  gradually  subside 
as  counter-irritants  are  used,  a  diagnosis  of  arterial  hyperemia  (aseptic) 
is  confirmed.  If  the  reaction  increase,  the  heat  become  more  irri- 
tating than  cold,  and  if  at  the  same  time  paroxysms  of  pain  or  reflex 
pain  occur,  the  diagnosis  is  that  of  venous  hyperemia  or  infective 
inflammation,  according  to  the  character  of  the  symptoms,  and  the 
pulp  must  be  removed.  In  cases  of  incomplete  roots  the  large  fora- 
men prevents  the  formation  of  a  venous  stasis.  Even  if  the  pulp  be 
kept  alive  only  until  root  completion,  much  good  will  be  done.  As  .an 
example,  in  one  case  a  lower  second  molar,  exposed  by  caries  and 
capped  at  the  age  of  fourteen,  at  twenty-five  years  reacts  as  vital 
to  an  interrupted  electric  current,  and  is  perfectly  comfortable. 

A  pulp  may  remain  quiescent  for  weeks  or  months  and  then  un- 
favorable symptoms  set  in,  or  it  may  die  without  any  apparent  pain. 
It  is  probable  that  in  the  latter  case  some  reflex  pains  have  been  felt, 
but  not  related  with  the  tooth,  in  the  mind  of  the  patient. 

In  the  successful  cases,  either  the  orifice  of  exposure  is  covered 
over  by  a  deposit  of  secondary  dentin,  or  the  pulp  remains  perfectly 
quiescent  beneath  the  capping  material,  without  formation  of  deposit. 

Even  when  a  deposit  occurs  the  pulp  may  die  from  the  atrophy 
and  degeneration  attendant  upon  the  formation  of  much  secondary 
dentin,  and  when  no  deposit  occurs  infection  following  leakages 
about  filling  and  capping  materials  may  take  place  after  years  of 
apparent  success.  While  capping  may  be,  and  has  been,  successful 
in  all  grades  of  exposure,  there  is  no  certainty  of  success  in  the 
exposure  by  caries.  The  tentative  treatment  necessary  offsets  the 
labor  of  canal  treatment.  The  alternative  to  capping  the  pulp  is 
its  removal.     This  requires  a  special  chapter  (which  see). 

THERAPEUTICS    OF   PERFORATION   BY   CARIES. 

The  progress  of  secondary  caries  in  the  dentin  about  the  pulp 
chamber  hollows  out  the  root  until  at  least  at  one  point  the  chamber 
wafl  is  but  a  decalcified  layer  of  cementum  covered  by  decomposing 
dentin.    At  some  point  the  pericemental  tissue  will  be  uncovered  by 


THERAPEUTICS  OF  PERFORATION  BY  CARIES 


429 


excavation  or  by  the  carious  process  (Fig.  378).  The  crown  will 
probably  be  badly  decayed.  Taking,  as  an  example,  a  lower  molar 
perforated  at  the  bifurcation  with  the  pericemental  tissue  hyper- 
trophied  into  the  opening  (fungous  gum),  its  treatment  may  be 
described  as  follows:    The  gum  is  first  to  be  pressed  out  with  cotton 


Fig.  378 


Fig.  379 


Diagram  of  treatment  of  perforation 
by  decay. 


Crowning  of  divided  roots.   (Evans.) 


medicated  with  an  antiseptic  varnish.  Fletcher's  carbolized  resin, 
or  aristol  in  chloroform,  or  sandarac  varnish  plus  orthoform,  will 
serve. 

If  immediate  work  be  desired,  polypoid  fungous  gum  may  be 
saturated  with  trichloracetic  acid  and  cut  away  without  bloodletting 


Fig.  380 


Fig.  381 


Cantilever  crown.   (Evans. i) 


Diagram  of  a  lateral  perforation  treated  with 
gutta-percha;  successful  for  seven  years,  when 
breakage  of  the  crown  occurred  including  the 
perforation:  GP,  gutta-percha;  OZ,  oxychlorid 
of  zinc;  A,  amalgam. 


by  means  of  a  large,  sharp,  spoon  excavator,  or  cocain  or  ethyl 
chlorid  may  be  used  for  local  anesthesia.  Large,  rose-head  burs  are 
used  to  free  the  cavity  of  all  decay.     The  canals  are  opened  and 


1  Artificial  Crown  and  bridge-work. 


430  DENTAL  CARIES 

treated.  If  further  treatment  be  desired,  or  be  impossible  until 
the  perforation  is  disposed  of,  metal  or  wooden  pegs  (the  Downie 
broach  reamers  will  serve)  are  placed  in  the  canals  and  a  reasonably 
thin  layer  of  copper  amalgam  is  built  about  the  pins  and  over  the 
perforation.  A  slight  movement  of  the  pegs  will  permit  their  with- 
drawal, leaving  openings  in  the  amalgam  through  which  the  treat- 
ment may  be  subsequently  conducted.  The  amalgam  is  then 
allowed  to  harden  (Fig.  378).  To  carry  on  the  treatment  while 
hardening,  formocresol  on  a  cotton  pellet  may  be  inserted  over  the 
openings  in  the  amalgam  and  sealed  over  with  soft  cement. 

After  canal  filling  the  canals  may  be  further  reamed  for  screws  or 
pins,  which  are  inserted  and  the  operation  completed  with  amalgam, 
or  zinc  phosphate  and  amalgam  if  the  condition  of  the  crown  admit 
of  it;  or,  if  crowning  be  required,  this  is  arranged  for  in  the  building 
up  with  amalgam. 

A  long  perforation  at  a  bifurcation  may  practically  divide  molar 
roots.  This  is  to  be  made  a  complete  division  after  treatment  of  the 
canals.  Each  section  may  be  fitted  with  a  pin  and  amalgam  stump, 
to  which  a  gold  barrel  is  fitted.  The  barrels  are  each  given  an  occlu- 
sal face,  or  the  two  a  common  occlusal  face,  and  soldered  together 
(Fig.  379). 

If  one  root  be  unsuitable  it  may  be  extracted  and  the  other  used 
as  a  foundation  for  a  cantilever  crown,  a  spur  from  which  rests 
slightly  upon  the  occlusal  face  of  the  adjoining  tooth  (Fig.  380),  or 
the  crown  may  carry  a  spur  which  rests  in  an  inlay  or  filling  in  the 
adjoining  tooth. 

A  smooth  plaque  of  low-heat,  white  gutta-percha  (not  temporary 
stopping)  makes  an  excellent  covering  for  a  perforation.  It  is  made 
larger  than  the  opening  covered,  warmed,  pressed  to  place,  and  the 
edges  sealed  with  a  hot  burnisher.  The  covering  filling  will  retain 
it  in  position.  The  approach  to  the  perforation  should  be  widely 
funnelled  to  permit  a  ready  adaptation.  A  splendid  covering  for 
accessible  perforations  is  found  in  oxyphosphate  of  copper  cement. 
The  opening  should  be  funnelled,  the  parts  dried  thoroughly  and 
the  cement  properly  mixed  can  be  painted  over  the  orifice,  adhering 
tenaciously  to  the  tooth  and  soft  tissue  without  pressure.  It  exer- 
cises an  antiseptic  influence.  If  sepsis  occur,  the  resulting  abscess 
will  occur  opposite  the  perforation,  or  in  some  cases  create  a  small 
pocket  similar  to  a  pyorrhea  pocket.  In  all  cases  judgment  must 
be  exercised,  and  the  attempt  to  conserve  unsuitable  cases  avoided 
(Fig.  381).     (See  also  Chapter  XX.) 


THERAPEUTICS  OF  LOSS  OF  CROWN  BY  CARIES         431 

THERAPEUTICS    OF   LOSS    OF    CROWN   BY    CARIES. 

If  the  portion  of  crown  left  after  excavation  be  self-sustaining, 
but  incapable  of  retaining  a  filling  in  the  cavity,  pins  or  screws 
may  be  placed  in  the  root  canal  or  the  pulp  cavity  may  be  enlarged 
and  made  retentive.  A  filling  is  then  built  about  or  into  the  anchor- 
age so  made.  At  times  the  remainder  of  a  tooth  crown  will  support 
a  hollow  metal  crown. 

When  the  carious  crown  has  broken  away  or  filling  has  become 
practically  impossible  or  undesirable,  the  original  beauty  or  useful 
form  of  the  tooth  may  be  approximately  restored  by  means  of  one  of 
the  many  forms  of  dowelled  porcelain  crowns,  specially  constructed 
gold  and  porcelain  crowns,  or  all-gold,  hollow-metal  crowns,  or  a 
broad  band  may  be  adjusted  and  filled  in  with  amalgam  after  setting 
with  cement,  or  where  a  portion  of  crown  only  remains  soft  amalgam 
may  be  used  inside  of  the  band  to  make  the  adaptation,  and  the  band 
then  filled  in,  completing  the  work  on  the  side  at  which  the  band 
has  no  cervical  adaptation.  These  operations  have  been  successful 
for  years,  if  the  remnant  of  crown  has  any  supporting  ability. 

If  an  anterior  root  be  so  hollowed  out  by  caries  as  to  be  incapable 
of  supporting  a  dowelled  crown,  with  or  without  a  cast  base,  it  may 
be  extracted,  and  the  operation  of  transplantation  performed,  or, 
later,  an  implantation  may  be  made. 

In  the  former  operation  the  existing  alveolus  is  enlarged  if  necessary 
to  accommodate  a  tooth;  in  the  latter  operation  a  new  alveolus  is 
created  by  means  of  appropriate  trephines  and  bone  reamers.  The 
tooth  is  to  be  prepared  as  for  replantation  (which  see).^ 

If  teeth  have  been  lost  by  extraction,  the  spaces  created  may  be 
filled  by  means  of  bridge-work  or  plates  of  various  sorts. 

By  common  consent  crown  and  bridge-work  is  considered  a 
special  department  of  dentistry. 

Therapeutics  of  Loss  of  Roots  by  Caries. — This  occurs  in  several 
ways : 

1.  After  loss  of  the  crown  and  the  extension  of  the  carious  process 
into  the  interior  of  the  root.  In  the  later  stages  this  root  is  rendered 
valueless  for  crowning  purposes,  and  should  be  extracted.  In  some 
cases  a  transplantation  operation  would  be  warrantable,  as  in  case- 
of  a  single  incisor,  the  other  teeth  being  relatively  sound.  (See  above.) 

2.  If  an  artificial  crown  has  been  so  placed  as  to  expose  the  joint 
to  caries,  the  process  may  proceed  to  a  considerable  extent,  but 
does  not  necessarily  involve  the  root  interior,  owing  to  the  presence 

1  For  methods  of  implantation,  see  American  Text-book  of  Operative  Dentistry. 


432  DENTAL  CARIES 

of  the  pin.  Filling  with  amalgam  or  other  plastic,  or  the  recrowning 
is  demanded  if  feasible.  The  gum  having  grown  in,  much  packing 
out  may  be  required;  ablation  may  be  required  as  well. 

3.  In  some  cases  penetrating  cervical  caries  will  cause  a  partial  or 
complete  amputation  of  a  lingual  or  buccal  root  of  an  upper  molar, 
or,  possibly,  a  bicuspid.  The  pulp,  of  course,  will  have  died,  at 
least  at  the  carious  area. 

The  cavity  of  decay  should  be  cleansed  and  undercut,  and  an 
occlusal  tap  made  for  free  entrance  to  the  canals.    The  canals  are  to 

be  reamed  with  Kerr  broaches.     The  canal 
Fig.  382  of  the  decayed  root  is  to  be  enlarged  with 

Kerr  root  reamers,  after  which  everything 
is  to  be  dried ;  a  canal  probe,  or  the  largest 
reamer  used,  which  may  have  wax  in  the 
spaces  between  the  blades,  is  passed  through 
the  tap  across  the  cavity  into  the  farther 
portion  of  the  root  canal.     Good  amalgam 
is  to  be  thoroughly  packed  into  the  cervical 
cavity  and  hardened  by  wafering.      When 
nearly  set,  the  filling  is  supported  against 
dislodgement  and  the  canal  probe  is  care- 
Method  of  restoring  lost     fully  withdrawn.    After  appropriate  steri- 
ZuM°hat"',S'or7';:t:S     ligation  of  canals  with  formalin  solutions, 
form  than  shown,  a,  amalgam,      the  canal  is  filled.     If  the  dccay  has  been 

severe,  and  fracture  threatens,  an  iridio- 
platinum  pin  is  to  be  fitted  into  the  involved  canal  and  the  crown 
tap  and  the  pin  used  as  the  canal  former  while  filling  the  cavity. 
Later  after  sterilization  it  is  cemented  into  the  canal,  thus  strength- 
ening the  root  against  a  threatened  fracture. 

If  actually  separated  by  decay,  excavation  will  make  an  open  joint, 
which  should  be  filled  with  amalgam  after  the  pin  has  been  run 
through  the  tap  into  the  root.  If  this  operation  does  not  seem 
feasible,  it  is  better  to  extract  the  separate  root  portion  and  trim  the 
stump,  as  in  ordinary  root  amputation. 

While  the  retention  of  an  amputated  root  is  seldom  demanded,  the 
editor  has  several  in  satisfactory  use.  The  prevention  of  a  threatened 
fracture  is  more  often  demanded.     (See  also  Heteroplasty.) 

CARIES    OF   THE   TEMPORARY   TEETH. 

Caries  of  the  temporary  teeth  differs  but  little  from  that  of  the 
permanent  teeth.  The  pulp  cavities  are,  however,  relatively  larger, 
and  the  intensity  of  the  carious  process  often  causes  rapid  exposure 


CARIES  OF  THE  TEMPORARY  TEETH  433 

of  the  pulp.  Owing  to  the  flat  character  of  the  approximations  of 
the  teeth,  there  is  often  more  approximal  than  occlusal  caries,  and 
the  cavities  often  have  weak  peripheries. 

Children  have  a  fear  of  dental  offices,  excited  by  unpleasant  experi- 
ences or  the  talk  of  their  elders,  and  they  do  not  mention  slight  pain 
such  as  that  excited  by  hypersensitive  dentin.  There  is,  however, 
abundant  evidence  that  the  dentin  of  the  temporary  teeth  may  be 
hypersensitive.  In  cavities  of  simple  nature  the  fillings  indicated 
for  adults  serve  if  the  operations  are  well  borne. 

The  shapes  of  the  teeth,  the  restlessness  and  fear  of  the  little 
patients,  and  the  free  flow  of  saliva  indicate,  for  the  most  part,  the 
use  of  plastic  fillings,  though  the  rubber  dam  may  often  be  readily 
used.  In  deep  cavities  not  exposing  the  pulps,  the  methods  employed 
for  adults,  of  varnishing  or  insulating  with  gutta-percha  and  the 
subsequent  use  of  zinc  phosphate  as  a  lining  under  metal  fillings, 
arei  ndicated.  (See  p.  421.)  Certain  occlusal  cavities  having  small 
orifices  and  large  interiors  are  well,  and  often  permanently,  filled 
with  pink  gutta-percha.  Zinc  oxid  and  eugenol  made  into  a  stiff 
paste  often  fills  cavities  acceptably,  and  lasts  as  well  as  oxyphos- 
phate  unless  it  is  too  freely  masticated  upon. 

If  cavities  are  observed  before  pain  has  been  complained  of,  and 
prompt  and  quickly  subsiding  response  to  applications  of  cold  water 
is  obtained,  indicating  a  normal  pulp,  the  cavity 
should  be  excavated,  with  more  regard  to  re-  ^^°-  ^^^ 

moving  the  marginal  caries  than  to  thorough  ,     /^C^ 

excavation,  dried,  and  an  application  of  a  20  |*^^t| 

per  cent,  solution  of  silver  nitrate  made  for  a  ^^^^ 

few  minutes,   the  cavity  being  subsequently  iS^I 

In   cases  of  adjoining   approximal    cavities         m  h       f 
there  is  a  disposition  for  the  affected  teeth  to     approximal  cavities. 
press  together  and  lessen  the  size  of  the  dental 

arch.  Bonwill  advised  as  a  practice,  followed  by  uniformly  good 
results  in  such  cases,  to  cleanse  the  cavities  (Fig.  383)  and  insert 
masses  of  pink  gutta-percha  base-plate.  The  constant  biting  upon 
the  gutta-percha  causes  a  separation  of  the  teeth,  which  increases 
the  size  of  the  arch  and  affords  additional  space  for  permanent 
successors.  Hollingsworth  introduced  the  idea  of  placing  a  small 
piece  or  cap  of  metal  at  the  cervix,  bridging  the  interdental  space. 
A  bit  of  gutta-percha  is  to  be  placed  on  the  under  side  of  the  cap 
to  make  a  gutta-percha  adaptation;  then  more  is  built  over  it.  Bon- 
will advised  that  before  the  gutta-percha  masses  are  inserted,  small 
pieces  of  blotting  paper  saturated  with  carbolic  acid  be  laid  against 
28 


434  DENTAL  CARIES 

the  dentinal  walls  and  the  gutta-percha  be  packed  over  them.  The 
more  efficient  and  persistent  antiseptic  silver  nitrate  may  be  applied 
instead  of  the  carbolic  acid.  Kirk  advises  that  asbestos  felt  be 
heated  to  destroy  any  organic  matter  present  in  it  which  might 
combine  with  the  silver,  and  then  be  soaked  in  a  saturated  solution 
of  silver  nitrate,  dried,-  and  kept  in  dark  bottles  away  from  the  light. 
Small  pieces  of  the  prepared  felt  may  be  used  as  described.  With 
cavities  as  good  as  shown  in  the  illustration,  wedging  and  contouring 
each  tooth  with  amalgam,  after  the  use  of  silver  nitrate  and  varnish, 
is  quite  admissible  after  making  suitable  retention.  There  is  no 
reason  why  occlusal  extension  for  retention  should  not  be  made. 
The  conditions  will  determine  the  choice  of  materials. 

Fig.  384 


Right  upper  temporary  molar  disked  lingually  and  filled. 

The  silver-nitrate  method  is  particularly  applicable  to  shallow 
cavities  in  which  excavation  for  filling  is  impracticable.  The  dentin 
surface  is  cleansed  and  dried,  and  the  fused  silver  nitrate  is  rubbed 
upon  the  surface.  This  may  be  done  after  the  method  of  Craven: 
a  platinum  wire  is  dipped  into  the  powdered  salt  and  held  over  a 
flame  until  the  powder  fuses  into  a  button.  By  this  hieans  applica- 
tion can  be  directly  and  accurately  made.  The  arch  is  apt  to  become 
somewhat  contracted,  and  food  is  liable  to  wedge  between  the  teeth. 
Combination  fillings  of  zinc  phosphate  or  oxyphosphate  of  copper 
and  amalgam  are  of  advantage  in  case  of  frail  walls. 


CARIES  OF  THE  TEMPORARY  TEETH  435 

For  the  anterior  teeth  siUcate,  zinc  phosphate,  and  gutta-percha 
fillings  are  useful,  and  for  the  posterior  ones  Ames'  oxyphosphate 
of  copper  serves  a  good  purpose. 

Caries  is  very  liable  to  occur  upon  the  approximal  surfaces  of  the 
second  temporary  and  first  permanent  molar.  If  the  former  be 
found  largely  decayed  distally,  the  latter  will  usually  be  found  decayed 
on  the  mesial  surface.  Amalgam  in  cavities  well  extended  buccally 
and  lingually,  or  gutta-percha,  serves  well  until  the  second  temporary 
molar  is  lost,  when  a  good  gold  filling  may  often  be  introduced 
before  the  second  bicuspid  erupts. 

Well-contoured  fillings  must  be  inserted  in  such  a  case.  As  a 
preventive  measure  during  eruption  of  the  first  molar,  the  second 
temporary  molar  may  be  disked  to  the  form  shown  in  Fig.  384. 

If  incipient  or  simple  decay  has  occurred  on  the  two  teeth,  or 
even  the  second  molar  alone,  it  is  then  best  to  wedge  the  teeth  apart 
and  to  make  a  disk  separation  (on  the  temporary  tooth  only)  from 
the  lingual  or  buccal  side,  or  both,  and  to  contour  the  filling  even  in 
exaggeration,  so  that  a  minimum  of  contact  shall  exist.  Any  sur- 
face of  dentin  exposed  by  the  disking  should  be  included  in  the  cavity, 
or,  if  this  be  not  possible,  then  it  should  be  rubbed  with  silver  nitrate. 

Such  surfaces  should  be  carefully  observed  at  regular  intervals; 
indeed,  if  prophylaxis  can  be  regularly  instituted  early  and  before 
caries  of  the  first  permanent  molar,  much  good  will  be  done. 

The  pulp  diseases  resulting  from  caries  of  the  temporary  teeth  wull 
be  considered  with  those  of  the  permanent  teeth.  If  the  temporary 
teeth  be  so  badly  decayed  as  to  be  hopeless,  so  far  as  filling  is  con- 
cerned, they  should  be  extracted.  Occasionally  the  encircling  of  the 
teeth  with  pure  gold  bands  cemented  to  place,  or  filled  in  with  amal- 
gam is  good  practice. 

In  the  main  the  temporary  teeth,  especially  the  molars,  should  be 
filled  with  some  view  to  the  longevity  of  the  fillings,  as  they  often 
have  to  do  service  for  years,  and  the  general  health  of  the  mouth  is 
improved. 

The  child  should  always  be  treated  with  kindness  and  truthfulness 
to  establish  faith,  yet  with  sufficient  firmness  to  command  control. 

Under  no  circumstances  should  the  child  be  given  an  excessive 
dread  of  dental  operations,  or  be  broken  by  nervous  shock,  as  this 
attitude  defeats  the  object  sought. 

In  one  extreme  case  in  which  the  child  had  never  endured  dental 
work,  chloroform  followed  by  ether  was  given  and  fifteen  plastic 
fillings  inserted.    N2O  and  O  might  be  used  for  the  purpose. 


436  DENTAL  CARIES 


RECURRENCE    OF   CARIES. 

Passing  over,  as  disproved  by  Miller,  the  theory  of  Palmer,  that 
caries  recurs  about  fillings  as  the  result  of  electric  action,  it  may  be 
stated,  as  proved  by  scientific  and  clinical  experience,  that  it  recurs 
because  after  teeth  have  been  filled,  conditions  exist  which  may  favor 
the  collection  of  microbic  plaques  and  stagnant  food  material  even 
more  strongly  than  the  original  conditions,  and  that  when  recurrence 
has  been  prevented,  the  work  has  been  done  in  such  a  manner  as  to 
prevent  such  collections 

The  specific  defects  which  favor  the  formation  of  bacterial  plaques 
may  be  epitomized  as  follows: 

1.  Lack  of  approximal  contact  (food  wedging  between  teeth). 

2.  Roughness  of  the  filling  at  an  otherwise  good  approximal  con- 
tact point  which  menaces  the  approximating  tooth  or  the  margin  of 
the  cavity  by  causing  food  retention  and  the  spreading  of  microbic 
plaques. 

3.  Unremoved  excess  of  filling  material  at  margins  producing  a 
ledge  which  collects  food,  etc.  The  edge  of  a  crown  may  act  in  a 
similar  manner.  An  excess  well  beneath  the  gum  is  more  apt  to 
produce  gingivitis  than  caries. 

4.  Exposure  of  the  cavity  margin  due  to  lack  of  covering  by  the 
filling  material,  whether  not  properly  placed,  flaked  away,  or  due  to 
fracture  of  margin  during  the  filling  process  or  subsequently  thereto. 

5.  Exposure  of  the  cavity  margin  due  to  shrinkage  or  shifting  of 
the  filling  material.  The  use  of  material  not  enduring  mastication 
in  places  subject  to  it;  the  washing  out  of  cement  from  the  joint 
of  an  inlay  or  combination  filling  or  dowelled  bandless  crown  has 
much  the  same  effect,  though  often  much  delayed. 

6.  Solubility  of  the  filling  material,  permitting  the  cavity  wall  to 
become  exposed. 

7.  Roughness  of  tooth  surface,  produced  by  polishing  fillings  with 
rough  approximal  trimmers,  coarse  grit  strips,  disks,  or  wheels. 
Exposure  of  dentin  by  overpolishing  may  be  classed  with  the  above. 

8.  Lack  of  hygiene  of  surfaces  which  tend  to  decay,  partly  due 
to  lack  of  extension  of  cavity  margins.  Even  poor  margins,  if  well 
extended,  may  not  decay,  whereas  existing  at  or  near  contacts  they 
are  menaces.  Lack  of  extension  of  approximal  cavities  often  causes 
failure,  through  failure  to  include  all  carious  enamel.  Lack  of  exten- 
sion of  a  filling  into  a  fissure  adjoining  it,  which  fissure  may  be 
decayed  or  invite  subsequent  decay.  Lack  of  extension  of  labial 
cavities  sufficiently  under  the  gum  cervically  and  in  the  mesial  and 


PROPHYLAXIS  OF  CARIES  437 

distal  direction,  leaves  a  tissue  vulnerable  to  microbic  plaques  if  not 
already  attacked  superficially. 

Treatment. — The  treatment  of  recurrent  caries  does  not  differ 
materially  from  that  of  primary  caries. 

Repairs  to  obliterate  crevices,  breaks,  or  new  decays  may  at  times 
be  made ;  but  so  often  is  it  the  case  that  apparently  slight  recurrences 
are  found  after  removal  of  the  filling,  to  involve  the  entire  cavity  wall, 
that  the  only  sound  recommendation  applicable  to  all  cases  is  that 
the  filling  be  removed  and  the  cavity  reprepared  and  refilled.  The 
exception  exists  when,  after  the  new  cavity  of  decay  is  all  excavated, 
the  adaptation  of  the  filling  is  seen  to  be  perfect.  Decay  at  two  or 
more  points  of  recurrence  not  subject  to  accurate  repair,  or  general 
inferiority  of  the  filling  should  condemn  the  entire  piece  of  work. 

PROPHYLAXIS    OF   CARIES. 

If  the  factors,  or  even  one  factor  of  caries  be  removed  from  the 
mouth,  caries  cannot  occur.  The  microscopic  plaques  and  fermen- 
table food  substances  acting  as  the  causes  of  caries  should,  therefore, 
be  kept  from  collecting  upon  the  teeth.  The  longer  they  remain, 
the  further  they  may  spread  laterally  over  the  tooth  surface. 

In  the  absence  of  absolutely  exact  knowledge  of  the  relation  of 
general  systemic  conditions  to  the  production  of  microbic  plaques,  it 
may  be  said  that  the  general  health  should,  if  possible,  be  maintained 
by  the  correction  of  any  morbid  body  state,  as,  without  doubt,  perfect 
good  health  is  a  corrective  of  morbid  oral  secretions.    (See  p.  356,  etc.) 

Apart  from  this,  oral  cleanliness  is  of  great  importance,  not  only 
for  the  health  of  the  teeth,  but  of  the  gums,  and,  indirectly,  of  the 
stomach  and  intestines,  which  can  but  be  affected  by  unhealthy  oral 
conditions.  Thus  while  the  general  health  may  influence  the  mouth, 
the  mouth  may  influence  the  general  health. 

It  has  been  noted  that  caries  is  markedly  lessened  in  well-kept 
dentures. 

The  first  step  in  the  prevention  of  caries  is  the  removal  of  all 
possible  causes  of  bacterial  plaque  formation.  Cavities  should  be 
obliterated  by  means  of  exactly  adapted,  perfectly  contoured,  highly 
polished,  insoluble  (in  so  far  "as  utilizable)  fillings,  the  margins  of 
which  are  extended  into  areas  subjected  to  friction  by  ordinary 
forces,  such  as  food  excursions,  brushing,  etc.  Departures  from  this 
principle  are  to  be  made  for  well-judged  reasons  only,  and  when 
made  prophylaxis  must  be  more  rigorous. 

Some  dentists  pursue  the  policy  of  filling  only  the  larger  cavities 
existing  in  a  mouth,  the  others  being  neglected  until  a  subsequent 


438  DENTAL  CARIES 

period.  Such  a  method  is  to  be  condemned  as  being  a  neglect  of  a 
plain  duty  and  as  tending  to  the  propagation  of  caries  in  the  mouth. 

Periodical  examinations  should  be  made  at  short  intervals,  pref- 
erably at  the  time  of  cleansing,  for  cavities  of  decay,  roughness  of 
filling  margins,  or  accidents  to  the  same.  By  these  means  the 
soil  may  be  rendered  unsuitable  to  the  growth  of  caries  fungi,  and 
their  localization  at  the  contacts  and  other  favoring  spots  is  largely 
prevented. 

Silver  nitrate,  40  per  cent,  to  saturated  solution,  may  be  applied  to 
surfaces  likely  to  decay,  as  sulci,  contact  points,  etc.,  as  a  means  of 
prevention  in  mouths  subject  to  same.^  As  a  systemic  and  local 
prophylactic,  the  diet  may  be  modified  (see  p.  361). 

The  presence  of  cavities,  calculus,  and  pyorrhea  alveolaris  in  the 
mouth  all  tend  to  cause  infection  of  the  digestive  tract,  with  produc- 
tion of  inflammatory  (catarrhal)  disturbance,  and  to  cause  infection 
of  parts  in  close  association  with  the  teeth  as  well. 

Undoubted  cases  of  septic  intoxication  and  infection  from  decayed 
teeth  and  other  oral  conditions  have  been  reported,  the  connection 
having  been  shown  by  their  cure  after  removal  of  the  local  cause 
alone;  in  other  cases  the  parts  (as  the  stomach)  having  the  secondary 
infection  well  implanted,  have  required  special  treatment  in  addi- 
tion to  the  removal  of  the  primary  exciting  cause. ^  (See  Systemic 
Effects  of  Pyorrhea  Alveolaris.) 

The  loss  of  masticatory  efficiency  due  to  caries  or  the  associate 
pain  has  a  direct  bearing  upon  insalivation  of  food  and  upon  gastric 
digestion,  though  in  this  connection  bacterial  infection  may  play  a 
part. 

School  children  who  suffer  much  from  caries  are  apt  to  be  less 
proficient  in  their  studies  than  normal  children,  the  effect  being 
probably  due  to  that  of  disturbed  digestion  upon  metabolism  and 
thus  upon  mentality  in  general.  Pain,  of  course,  is  a  direct  cause 
reducing  vitality  in  various  ways  and  causing  loss  of  time  and  atten- 
tion to  the  duty  of  study,  etc.  The  following  quotation  from  a 
tabulation^   shows  typically  the   effect  of  dental  normality  upon 

1  L.  C.  Bryan  and  others. 

2  Hunter:  International  Dental  Journal,  1899,  abstract  from  Transactions  of 
Odontological  Society  of  Great  Britain. 

In  an  address  at  McGill  University,  Montreal,  Hunter,  1910  (see  Dental  Brief, 
November,  1911).  reaffirms  extensive  experience  with  gastritis,  septic  anemia,  septic 
endocarditis,  etc.,  as  the  result  of  oral  sepsis  in  which  decayed  roots  and  extensive 
dental  work,  (bridge,  etc.) ,  covering  septic  conditions  were  cured  by  removal  of  the 
cause.  While  caries  was  not  separately  considered,  it  must  be  seen  that  caries  is 
largely  responsible,  as  the  inception  of  the  conditions  through  pyorrhea  is  also 
responsible. 

3  Dental  Brief,  1911.  Tabulation  of  the  Effects  of  Dental  Caries  on  the  Mental 
Powers  of  the  Dental  Class  in  Marion  School,  Cleveland,  Ohio. 


Per  cent,  of 

Present. 

Diffeience. 

gain  or  loss. 

66.6 

00.05 

00.07 

90.7 

16.50 

22.22 

63.0 

17.00 

36.95 

92.0 

33.00 

55.93. 

60.5 

19.00 

45 .  78 

DAILY  CLEANSING  OF  THE  TEETH  439 

mental  powers.     It  has  the  lowest  gain,  which  ranged  from  about 
32  to  about  918  per  cent. 

Beginning. 

Memory 66.65 

Spontaneous  association        .       .      .      .74.25 

Addition .      .      .46.00 

Association  by  opposite         .      .       .       .      59 .  00 
Quickness  and  accuracy  of  perception      41.50 

Total  gain      ....      32.162  per  cent,  after  deducting  the  losses. 

Insomnia  and  a  variety  of  other  metabolic  ills  have  been  shown 
to  be  due  to  carious  teeth  and  the  sepsis  associated,  by  the  prompt 
or  gradual  recovery  upon  removal  of  the  teeth.  How  many  thous- 
ands of  individuals  suffer  from  partial  sepsis,  in  entire  ignorance  and 
possibly  without  actual  discomfort  can  only  be  conjectured.  It  is 
exceedingly  difficult  to  state  positively  that  a  metabolic  disorder 
is  due  to  the  state  of  the  mouth,  unless  a  microscopic  examination 
from  a  separate  locality  demonstrates  identical  bacteria  present. 
Even  then  the  therapeutic  test  must  decide.  Therefore  general 
deductions  must  govern  advice.  In  all  cases  it  is  wise  to  put  the 
mouth  into  a  hygienic  state  and,  if  necessary,  add  such  other  therapy 
as  the  systemic  condition  demands. 

The  evils  attendant  upon  sepsis  are  to  be  pointed  out  to  patients 
who  have  often  a  seeming  indifference  to  conditions  ranging  from 
simple  uncleanliness  to  loathsome  filth  within  the  mouth,  which 
would  alarm  them  if  existing  in  any  other  part  of  the  body.  Aside 
from  all  considerations  of  health  or  tooth  integrity,  it  is  poor  economy, 
and  especially  for  poor  people,  to  neglect  these  measures  which  are 
largely  applicable.  The  prophylaxis  of  the  teeth  apart  from  periodical 
cleansings  is  a  matter  for  careful  instruction  and  exhortation  of 
patients  who  are  apt  to  be  persistent  backsliders.  Indeed,  it  is  the 
opinion  of  the  writer  that  most  patients  accept  the  validity  of  the 
arguments  herewith  presented  and  then  persistently  neglect  or  even 
frankly  refuse  to  carry  out  the  treatment.  It  is  therefore  no  surprise 
that  caries  persists.  The  deduction  may  be  made  that  the  cleansing 
of  teeth  at  spots  that  ordinarily  do  not  decay  is  nearly  equivalent 
to  no  brushing  at  all. 

DAILY    CLEANSING    OF    THE    TEETH. 

A  small,  well-made,  fairly  stiff  brush,  having  its  brushing  surface 
serrated,  is  to  be  grasped  in  the  palm  of  the  hand  with  the  ball 
of  the  thumb  placed  upon  the  back  of  the  handle,  or  exactly  the 
reverse,  according  to  the  movement  desired.     The  bristles   are  to 


440 


DENTAL  CARIES 


be  passed  over  the  buccal  and  lingual  surfaces  of  the  teeth,  from  the 
gum  toward  the  occlusal  surfaces,  by  means  of  a  dexterous,  wiping 
motion  imparted  by  a  turn  of  the  wrist.     Figs.  385,  386,  and  387 


Fig.  385 


Fig.  386 


Fig.  3S7 


by  S.  Blair  Luckie,  show  this.  This  cleanses  the  interproximal 
spaces  so  far  as  accessible  to  the  brush.  By  a  light  to-and-fro 
motion,  spreading  the  bristles  over  the  cervices,  the  lingual  and 
buccal  cervices  are  freed  of  soft  deposits  which  occur  after  each  meal. 


DAILY  CLEANSING  OF  THE  TEETH  441 

Unless  the  gums  be  actually  torn,  this  light  friction  is  not  injurious. 
Special  attention  is  to  be  paid  to  the  buccal  surfaces  of  third  molars, 
which  are  often  ignored  even  by  conscientious  patients.  This  is  due 
to  a  habit  of  giving  a  downward  sweep  of  the  brush-tip,  which  escapes 
the  rather  upwardly  placed  third  molar. 

The  lingual  surfaces  of  incisors  are  cleansed  by  means  of  the 
tip  of  the  brush.  In  cases  of  advanced  recession  of  the  gum  about 
incisors,  a  brush  with  all  the  bristles  except  those  of  the  tip  cut  away 
(and  the  stubble  ground  down)  is  advantageous.  This  is  also  useful 
for  the  lingual  surfaces  of  bridge-work.  Occlusal  surfaces  are  to  be 
freely  brushed.    Brushes  of  this  form  can  be  purchased. 

A  light  brushing  after  each  meal  imparts  to  the  mouth  a  pleasing 
sense  of  cleanliness,  which  has  a  good  moral  effect  upon  the  patient, 
and  removes  from  about  the  teeth  much  fermentable  material. 

The  teeth  should  be  thoroughly  brushed  upon  retiring,  to  remove 
any  debris  about  the  teeth.  A  small  rubber  band  should  be 
stretched  between  the  teeth,  the  inner  end  released,  and  then 
drawn  through  the  interdental  space,  wiping  the  approximal  sur- 
faces and  embrasures.  This  places  the  mouth  in  a  fairly  aseptic 
state  for  the  night,  during  which  the  oral  fluids  are  at  rest  and 
less  interfere  with  fermentation,  or  neutralize  its  products.  The 
brush  itself  should  be  sterilized  after  using.  A  good  glass  brush- 
holder  is  sold  which  has  a  small  portion  of  paraform  placed  in  the 
lower  part,  and  is  capped  with  a  metal  screw  cap.  In  this  the  brush 
may  remain  until  again  needed. 

Before  breakfast  the  teeth  should  again  be  brushed. 

Once  a  week  the  patient  should  rub  tooth  powder  over  the  inter- 
proximal spaces,  and  carry  floss  silk  between  the  teeth  and  rub  the 
approximal  surfaces,  with  the  object  of  removing  any  bacterial 
collections  upon  these  surfaces. 

The  floss  silk  should  not  be  forced  into  the  gum,  as  this  will  injure 
the  gum  margins  and  force  infected  material  into  it,  but  should  be 
first  carried  gently  beneath  the  gum,  wrapped  half  around  the  tooth, 
and  then  sawed  up  over  the  contacts  and  be  brought  out  from 
between  the  teeth.  It  should  be  reintroduced  at  the  same  interspace 
and  the  adjoining  tooth  polished.  This  use  of  floss  still  leaves  at 
the  middle  of  the  buccal  and  lingual  cervix  a  point  often  uncleansed 
(see  Fig.  364).  The  use  of  the  brush  to  accomplish  this  should 
be  taught,  otherwise  cervical  caries  may  supervene  (see  p.  384). 

The  lingual  surface  of  lower  incisors  may  usually  be  accurately 
flossed  by  throwing  the  floss  around  a  single  tooth,  then  crossing 
the  strands  and  pulling  on  each  alternately.  This  cleanses  the 
entire  circumference  at  the  cervix,  as  the  floss  tends  to  go  cervically 


442  DENTAL  CARIES 

under  such  a  manipulation  as  is  shown  by  its  use  with  the  rubber  dam. 
If  there  is  any  difficulty  in  the  use  of  floss,  it  is  due  to  faults  about 
the  approximal  surface  which  should  be  remedied.  In  cases  of  lower 
incisors  collecting  calculus  readily  this  may  have  to  be  done  daily. 

The  twisted-wire  bodkin  shown  in  Fig.  389  is  very  valuable  as  a 
means  of  threading  the  floss  through  a  bridge  space.  Being  readily 
bent  into  a  half-circle  it  returns  toward  the  lips  so  as  to  be  readily 
grasped.  It  should  be  bent  in  line  with  the  flatness  of  the  eye.  To 
make  them,  take  the  temper  from  a  thin  shank  like  that  of  an  old 
Gates  Glidden  drill,  bend  it  into  the  form  of  a  button-hook;  over 
this  loop  a  six-inch  length  of  fine  regulating  wire.  Revolve  the  hook 
in  the  engine  and  run  the  wire  through  the  fingers  of  the  left  hand. 

The  periodical  cleansing  or  prophylaxis  suggested  by  D.  D.  Smith 
involves  the  monthly  rubbing  down  of  all  surfaces  accessible,  to  a 
wedge-shaped,  wooden  polishing  point  carried  in  a  Jack  porte. 
Powdered  pumice  is  the  abrasive  suggested.  The  point  is  to  be  gently 
insinuated  beneath  the  free  gum  margin  for  the  purpose  of  effecting 
a  cleanliness  there,  which  shall  prevent  collections  liable  to  produce 
pyorrhea  alveolaris.     (See  Fig.  645.) 

This  method  may  be  supplemented  by  a  careful  rubbing  down  of 
contact  points  and  embrasures  by  means  of  floss  silk,  charged  with 
powdered  pumice  as  an  additional  precaution  against  approximal 
caries. 

Fig.  388 


Simple  porte-polisher.     One,  shoe  peg  trimmed. 

The  slight  cleansing  apparently  required  after  a  few  visits  is  a 
strong  argument  in  favor  of  these  prophylactic  cleansings,  and  chalk 
may  be  substituted  for  the  pumice.  In  case  of  fairly  clean  mouths, 
free  of  other  disease  than  caries  the  patient  may  be  instructed  in 
the  use  of  a  shoe  peg  sharpened  to  a  point,  held  in  a  simple  porte- 
polisher,  such  as  a  tube  of  thin  nickelled  brass  bent  at  one  end  to  an 
angle  of  45  degrees  (Fig.  388),  and  the  prophylaxis  by  the  operator 
executed  three  or  four  times  a  year  only.  This  wood  point  is  useful 
in  cleansing  the  lingual  surfaces  of  bridge-work. 

It  is  exceedingly  difficult  to  instruct  patients  in  the  proper  use 
of  the  wood  point,  but  once  properly  instructed  the  results  are 
little  short  of  marvelous.  In  use  it  is  to  be  held  in  the  hand  as 
though   using   the   Spencerian   system  of  penmanship.     The  third 


DAILY  CLE A-N SING  OF  THE  TEETH  443 

and  little  finger  rest  upon  the  chin  or  teeth  as  a  fulcrum.  The 
point  is  first  adjusted  at  the  distal  of  the  third  molar  and  with  a 
rocking  motion  of  the  hand  it  is  drawn  along  the  cervix.  The  rule 
is  to  "keep"  on  the  tooth  but  "feel"  the  gum.  Jumping  from  the 
buccal  of  one  tooth  to  another  is  to  be  avoided.  The  point  should 
be  deliberately  but  gently  drawn  (not  rubbed),  until  it  rests  in  the 
interspace.  Next  the  fulcrum  fingers  are  slightly  shifted  and  the 
next  tooth  cleansed. 

Fig.  389 


Flexible  wire  bodkin  slightly  enlarged. 

When  the  anterior  teeth  are  reached,  the  patient  should  begin 
again  at  the  third  (or  last)  molar  of  the  opposite  side.  The  motion 
is  repeated  upon  the  lingual  surface.  In  no  case  should  sight  be 
depended  upon.  The  sensation  of  contact  is  the  best  guide.  As  a 
means  of  instruction  of  the  patient,  tincture  of  iodine  and  alcohol 
equal  parts  should  be  applied  and  then  washed  off  with  water.  The 
films  will  stain  for  a  short  time,  during  which  the  effect  of  the  fric- 
tion of  floss  and  stick  and  the  inefficiency  of  the  usual  brushing 
can  be  demonstrated.  If  desirable,  the  patient  may  occasionally 
use  the  stain  as  a  means  of  self  instruction. 

The  Dentifrice. — There  is  no  contention  as  to  the  value  of  friction 
and  the  removal  of  the  factors  of  caries,  but  of  late  the  character 
of  dentifrice  to  be  used  has  been  brought  into  question. 

Pickerill  has  contended  that  antiseptics  are  of  doubtful  value  and 
that  ordinary  alkaline  dentifrices  depress  the  flow  of  saliva  and  that, 
on  the  other  hand,  an  acid  dentifrice,  as  acid  potassium  tartrate  in 
1  to  200  solution,  increases  the  flow  of  alkaline  saliva,  which  being 
continuous  neutralizes  any  acid  formed.  As  aside  from  a  detergent 
action,  alkalinity  is  the  object  sought  in  a  dentifrice,  the  method 
seems  rational,  especially  as  he  has  found  that  the  acid  does  not  injure 
the  teeth. 

Of  his  formulae  the  following  is  said  to  be  the  most  agreeable: 

I^ — -Potassii  bitartratis  (P.  tartratis  acidi,  B.  P.)      .       .      .      gr.  ij 

Aeidi  tartarici gr.  j 

Olei  limonis lU  iij 

Glusidi  (saccharini) gr.  ; 

AquiB       .      ."      . ad  fgj — M. 


444  DENTAL  CARIES 

The  contentions  of  Pickerill  are  based  upon  his  observations  of 
immunes,  and  experiments  which  curiously  enough  do  not  seem  to 
include  definite  experimental  applications  to  any  particular  indi- 
vidual susceptible  to  caries.  It  is  seemingly  becoming  the  fashion 
to  claim  that  prophylaxis  is  a  failure  (Pickerill  admits  its  occasional 
value),  which  will  not  be  admitted  for  a  moment  by  any  one  who 
has  conscientiously  performed  it  each  three  months,  or  oftener,  with 
reasonable  assistance  from  the  patient  (see  footnote  p.  358).  Anti- 
septics are  also  denied  a  value,  but  even  Pickerill  admits  their  value 
in  oral  sepsis,  so  why  can  they  be  valueless  in  caries.  They  produce 
a  disturbance  in  the  medium,  slight  changes  in  which  are  known  to 
affect  bacteria,  a  fact  taken  advantage  of  by  Pickerill  as  a  claim  for 
acid  value.  If  disturbance  of  medium  is  of  value,  the  frequent  break- 
ing up  of  plaques  theoretically  should  be  of  immense  value  and  in 
practice  so  proves. 

Antiseptics  have  been  shown  to  reduce  general  oral  infection  to 
a  possible  minimum  when  oral  cleanliness  is  conjoined  with  their 
faithful  use,  but  without  exact  prophylaxis  cannot  be  depended  upon. 

The  writer  has  found  phenol  sodique,  1  to  7  of  water,  a  useful 
adjunct  in  this  connection  and  as  an  occasional  germicide  to 
promote  the  action  of  milder  antiseptics,  the  following  mercuric 
chloride   wash   used   for   the  space   of    two    minutes   is   valuable:^ 

I^ — Mercuric  chlorid gr.  vj 

Thymol gr.  i.j 

Menthol gr.  v 

Oil  eucalyptus gtt.  x 

Glycerin fgij 

Alcohol fgij 

AuQEe  gaultherige .'     .      q.  s.  ad.  Oij — -M. 

S. — Use  as  directed  as  mouth  wash. 

The  writer  has  found  much  value  in  the  use  of  a  potassium  chlorate 
paste.  This  certainly  has  kept  black  stain  from  teeth  which  usually 
accumulated  strong  evidence  of  it  within  two  weeks  of  prophylaxis, 
and  caries  is  apparently  much  lessened  by  its  use  though  prophy- 
laxis is  a  confusing  factor.  Potassium  chlorate  has  been  condemned 
by  dentists  of  high  standing  as  systemically  injurious,  but  whether 
such  small  doses  as  might  be  swallowed  after  tooth  cleansing  could 
be  injurious  has  not  been  scientifically  shown.  On  the  other  hand 
experiments^  have  been  made  on  puppies  which  received  thirty  grams, 
daily  for  six  weeks,  were  then  killed  and  no  renal  lesions  were  found ; 
the  gastric  mucosa  showed  no  signs  of  irritation  nor  the  blood  any 
methemoglobinemia,  and  the  animals  showed  normal  growth.    While 

1  C.  R.  Jackson,  Dental  Summary,  1904. 

2  Medical  Brief,  December,  1912. 


DAILY  CLEANSING  OF  THE   TEETH  445 

large  doses  may  have  been  injurious  to  humans  this  is  entirely  different 
from  minute  residue  in  the  mouth.  As  a  matter  of  fact,  if  the 
mouth  be  washed  out  with  water  no  appreciable  toothpaste  need  be 
swallowed. 

The  use  of  chewing  gum  after  meals  has  been  of  value  in  suscep- 
tibles.  Either  it  acts  by  friction,  removing  fermentable  food  or  by 
promoting  a  free  flow  of  saliva;  perhaps  in  both  ways. 

Whether,  however,  it  shall  be  best  in  the  future  to  prescribe 
a  weak  organic  acid  as  a  dentifrice  and  trust  to  the  flow  of  alkaline 
saliva  or  use  a  weak  alkaline  wash,  as  lime-water  one-half  strength, 
or  even  an  alkaline  tooth  powder  or  paste  must  be  decided  by  actual 
clinical  experiment  upon  susceptibles,  as  immunes  are  valueless  for 
observation  unless  they  lapse  from  immunity.  Even  here  the  credit 
must  not  be  given  altogether  to  the  acid  treatment  side  of  the  con- 
tention unless  prophylaxis  is  eliminated.  In  brief,  the  whole  sub- 
ject requires  intelligent  ventilation.  We  have  to  thank  Picker  ill 
and  Gies,  working  on  this  line,  for  at  least  a  new  departure  in  our 
thinking  regarding  dentifrices. 

By  these  means  centres  of  infection  are  removed,  and  the  problem 
is  reduced  to  the  care  of  the  superficies  of  the  teeth.  Calculus  should 
be  thoroughly  removed,  the  teeth  highly  polished  and  kept  polished. 
This  operation  mechanically  removes  the  plaques. 

To  prevent  their  return,  daily  cleansing  of  the  teeth  by  the  patient 
has  always  been  practised,  and  a  thorough  cleansing  once  a  month 
or  oftener  by  the  operator  has  been  shown  by  D.  D.  Smith  to  be 
highly  efficacious.  The  patient  should  be  instructed  regarding  the 
location  of  the  plaques  producing  dental  disease.  A  good  method  is 
to  apply  tincture  of  iodin  to  the  teeth,  then  douche  them  with  water, 
which  removes  the  iodin  from  the  clean  part.  The  teeth  will  gener- 
ally then  look  like  Fig.  321,  which,  while  a  figure  of  decay,  will  take 
the  place  of  a  special  illustration.  While  thus  stained  the  effectiveness 
of  floss,  etc.,  can  be  readily  demonstrated.  Inasmuch  as  caries  is 
usually  prevented  by  a  thorough  monthly  prophylaxis  followed  by 
oral  hygiene  at  the  hands  of  the  patient,  it  follows  that  if  the  bacterial 
plaque  is  frequently  disturbed  the  most  important  link  in  the  chain 
of  factors  is  eliminated.  Even  if  a  systemically  produced  carbohy- 
drate should  be  shown  to  be  a  factor  as  food  supply  for  bacteria, 
it  can  produce  no  injury  alone,  while  it  is  probable  that  bacteria 
plus  extraneous  carbohydrate  is  competent  to  produce  caries. 

Finally  a  dietary  should  be  outlined  which  shall  be  proper  for 
general  health,  shall  reduce  the  carbohydrate  element  remaining  in 
the  mouth  (as  candy  and  cracker  consumption  between  meals), 
and  shall  induce  a  flow  of  alkaline  saliva  after  meals  (see  p.  361). 


446  DENTAL  CARIES 

PROPHYLAXIS   IN   SYSTEMIC   DISEASE. 

During  a  prolonged  illness,  seasickness,  pregnancy,  etc.,  the  pro- 
phylaxis of  the  teeth  should  be  as  rigidly  enforced  as  possible  as  a 
means  of  preventing  decay  of  the  teeth  and  sepsis  of  the  mouth. 

It  has  been  shown  that  during  pregnancy  osteomalacia  may  occur, 
and  that  it  represents  a  demineralization  by  decalcification  of  the 
bones  of  the  mother.  Whether  or  not  this  may  influence  caries  of 
enamel  is  not  certain,  though  acid  secretions  occur  from  the  gum 
margins,  but  there  is  no  reason  why  the  resistance  of  the  fibrils  of 
the  dentin  should  not  be  lessened,  or  even  that  the  dentin  may  not 
be  to  an  extent  demineralized,  as  positively  claimed  by  some  accurate 
observers  (Black  to  the  contrary).  An  excessive  osteomalacia  may 
be  held  to  represent  a  deficiency  of  osteogenetic  nutritive  material 
for  the  child.  This  would  lead  to  an  inferior  development  of  the 
child's  temporary  teeth. 

Any  abnormal  condition  of  the  mother  should  be  corrected,  ■  if 
possible,  in  order  that  her  general  nutrition  and  that  of  the  child 
may  not  suffer. 

Probably  upon  the  congenital  constitution  of  the  child  depends 
much  of  its  future  susceptibility  or  immunity  to  caries. 

Accepting  the  decalcification  theory  of  osteomalacia,  the  use  by 
the  nursing  or  gravid  mother  of  mild  alkalies  internally,  such  as  a 
tablespoonful  of  lime  water  repeated,  and  the  use  of  lime-containing 
foods,  as  the  cereals,  and  mineral  waters  as  beverages,  cannot  but  be 
of  values  as  antacids  furnishing  a  neutralizing  agent  for  the  acid, 
while  the  lime  probably  enters  into  the  development  of  bone  (Hare) , 
and,  therefore,  would  be  useful  in  supplying,  via  the  placenta, 
mother's  milk,  and  later  the  child's  food,  the  element  needed  for  the 
development  of  teeth.  The  use  of  glycerophosphate  of  lime  and  soda 
has  been  suggested. 

The  teeth  should  receive  all  needful  care  during  pregnancy,  that 
the  mother  should  not  suffer  pain,  but  work  should  be  of  a  temporary 
nature,  if  necessary,  to  avoid  shock,  especially  at  about  the  third 
month  of  gestation.  Attention  has  been  called  to  the  fact  that 
during  menstruation  a  systemic  hyperacidity  exists,  which  can  be 
combated  by  the  use  of  lime  internally  and  milk  of  magnesia  or 
lime  water  locally. 

In  the  care  of  the  teeth  during  pregnancy  the  effect  of  the  hydro- 
chloric acid  vomitus  upon  the  teeth  should  be  considered,  an  alkaline 
wash  such  as  lime  water  or  bicarbonate  of  soda  solution  to  be  used 
after  the  vomiting.  The  same  would  be  true  of  seasickness  and  after 
the  use  of  any  acid  drug  or  foodstuff,  such  as  tincture  of  ferric  chloride 
or  buttermilk  in  case  the  latter  is  a  constant  diet.    (See  p.  354). 


SECTION  lY. 

DISEASES  OF  THE  DENTAL  PULP. 


CHAPTER  XV. 
CONSTRUCTIVE  DISEASES. 

Diseases  of  the  dental  pulp  are  both  acute  and  chronic.  Accord- 
ing to  the  anatomical  features,  they  may  also  be  divided  into  con- 
structive and  destructive.  The  acute  diseases  are  usually  destruc- 
tive; in  the  chronic,  structural  and  constructive  changes  are  com- 
monly noted.  Constructive  diseases  of  the  dental  pulp  are  those 
attended  by  the  formation  of  deposits  of  new  masses  of  calcific 
substance.  Destructive  diseases  are  those  which  cause  retrogressive 
and  necrotic  changes  in  the  tissues  of  the  pulp.  The  essential  differ- 
ence between  the  two  classes  of  disease  is  in  the  mode  and  character 
of  the  degeneration — the  one  is  acute,  the  other  chronic. 

Pathologically  there  is  no  abrupt  line  of  demarcation  between 
diseases  of  the  dentin  and  those  of  the  pulp,  as  the  dentinal  tubules 
contain  the  fibrillar  prolongations  of  the  odontoblasts  of  the  pulp. 
Effects  produced  upon  the  fibrils  cause,  therefore,  a  pulp  reaction 
which  may  lead  either  to  a  constructive  or  destructive  activity 
according  to  the  grade  of  hyperemia  or  inflammation  set  up. 

As  infection  may  travel  via  the  tubules,  even  septic  inflammation 
may  result  before  the  pulp  is  exposed. 

Moreover,  after  constructive  changes  which  are  accompanied  by 
more  or  less  atrophy  and  degeneration,  ,the  pulp  may  undergo  the  more 
acute  destructive  changes.  While  the  exact  relations  between  symp- 
toms and  pathology  are  not  all  worked  out  and  the  symptoms  are 
often  obscure,  due  to  the  fact  that  the  pulp  is  without  the  sense  of 
touch  or  exact  location,  and,  therefore,  the  pains  induced  are  reflected, 
as  a  rule,  yet  clinical  observation  and  the  .r-rays  have  done  much  to 
relate  the  symptoms  and  pathology,  and  one  must  depend  upon 
these  and  applied  tests  for  at  least  a  tentative  diagnosis,  of  which 
confirmation  may  be  sought, 

(447) 


448       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

The  pathological  conditions  of  the  pulp  are  judged  by  the  phenom- 
ena induced  by  applications  of  air  or  water  of  varying  temperatures, 
and  by  the  presence  of  certain  appearances  of  the  tooth,  which,  taken 
with  the  symptoms  and  tests,  lead  to  a  fair  inference  of  the  disease 
present. 

It  was  pointed  out  by  Black^  that  if  a  healthy  tooth  be  isolated  by 
a  double  layer  of  rubber  dam,  and  a  jet  of  water  at  a  temperature  of 
40°  F.  be  directed  against  the  tooth,  a  paroxysm  of  pain  is  produced. 
A  jet  of  hot  water  will  also  induce  a  similar  pain,  and  if  the  patient's 
eyes  be  shielded  no  difference  in  the  sensations  is  noted;  that  is, 
the  pulp  responds  to  thermal  stimuli,  hot  or  cold,  indifferently.  The 
organ  is  accustomed  to  variations  of  temperature  between  60°  and 
105°  to  110°  F.,  and  within  this  range,  in  a  condition  of  health, 
takes  no  apparent  cognizance  of  this  degree  of  change. 

With  a  decrease  in  the  amount  of  dentin  covering  the  pulp — e.  g., 
with  the  advance  of  caries — the  reaction  to  thermal  stimuli  increases 
in  promptness  until,  when  the  pulp  is  nearly  exposed,  the  response  is 
immediate.  As  the  pulp  irritation  increases  there  is  prompt  response 
to  lesser  degrees  of  temperature  change,  until  finally  the  pulp 
responds  immediately  to  water  at  a  temperature  but  a  few  degrees 
below  or  over  the  bodily  temperature,  98.6°  another  feature  makes 
its  appearance;  instead  of  a  sharp  contraction  pain,  applications 
of  moderate  thermal  stimuli  are  followed  by  a  heavy,  throbbing 
pain.  Later,  similar  pains  occur  in  the  absence  of  tangible  external 
sources  of  irritation.  In  conditions  of  abscess  intense  pain  is  later 
caused  by  hot  applications,  and  cold  applications  afford  relief. 

In  pulp  degeneration  the  response  to  thermal  stimuli  may  pursue 
the  opposite  course.  The  normally  prompt  response  is  followed  by 
delays  in  reaction,  until  it  is  only  after  the  continued  application  of 
cold  to  the  exterior  of  a  tooth  that  a  paroxysm  of  pain  is  induced. 
In  these  cases  there  follows  after  a  relatively  long  time  an  increasing 
response  to  heat,  as  in  the  former  instance,  the  reaction  occurring 
ortly  upon  decided  or  prolonged  heat  stimuli.  Following  upon  the 
period  of  increased  response  to  heat,  in  both  cases  there  comes  a 
period  of  quiescence,  in  which  there  is  no  response  whatever  to 
applications  of  intense  cold,  even  that  produced  by  the  evaporation 
of  a  spray  of  ethyl  or  methyl  chlorid — i.  e.,  the  sensory  function  of 
the  pulp  is  paralyzed.  This  only  in  intense  venous  hyperemia  or 
degeneration. 

These  are  the  available  subjective  evidences  of  the  pathological 
conditions  of  the  pulp;  while  they  indicate  with  a  degree  of  accuracy, 

1  American  System  of  Dentistry,  vol.  i. 


TUBULAR  CALCIFICATION  449 

useful  in  clinical  work,  the  alterations  in  the  pulp,  the  exact  relations 
between  the  reactions  and  the  morbid  anatomy  of  the  organ  are  not 
entirely  clear.  It  is  assumed  that,  in  consequence  of  the  loss  of  the 
normal  protective  covering  of  the  pulp,  its  sensory  and  perhaps 
vasomotor  nerve  fibres  become  stimulated,  overstimulated,  irritated, 
and  then  paralyzed  by  thermal  stimuli  in  the  progress  of  caries.  The 
bloodvessels,  which  retained  their  tone  up  to  a  certain  point,  suft'er 
vasomotor  irritation;  next,  paralysis  leading  to  their  dilatation  and 
to  the  throbbing  pain.  Later,  even  change  of  posture  is  sufficient  to 
cause  distention  of  the  paralyzed  vessels,  hence  pain  in  resuming 
the  reclining  position.  Stimulation  by  cold,  until  the  later  stages, 
causes  a  sharp,  continuous  pain,  ascribed  to  the  paroxysmal  con- 
traction of  the  vessels.  In  the  stages  of  paralysis  heat  causes  further 
distention  of  the  vessels,  and,  if  gases  be  present,  causes  their  expan- 
sion with  pressure  upon  nerve  filaments. 

The  decreasing  and  delayed  response  to  thermal  stimuli  must  be 
referred  to  three  sources:  (1)  An  increase  in  the  non-conducting 
covering  of  the  pulp — i.  e.,  a  lessening  of  the  amount  of  the  fluid 
contents  of  the  dentinal  tubuli  and  a  thickening  of  the  dentinal  walls, 
which  necessarily  implies  a  recession  of  the  pulp  from  its  normal 
position;  (2)  to  degeneration  of  the  sensory  nerve  fibers  themselves; 
and  (3)  changes  in  the  walls  of  or  about  the  bloodvessels,  which  check 
vasomotor  response  and  changes  in  the  caliber  of  the  vessels.  These 
three  classes  of  reactions  still  fifrthe'r  emphasize  the  division  of  the 
pulp  diseases  into  two  types,  the  acute  and  chronic;  the  first  class  of 
reaction  is  associated  with  the  acute  destructive  diseases ;  the  second, 
with  the  chronic  constructive  but  degenerative  conditions. 

CONSTRUCTIVE   DISEASES    OF    THE   DENTAL   PULP. 

The  constructive  diseases  of  the  dental  pulp  include  all  the  sec- 
ondary dentin  formations,  tubular  calcification,  the  formation  of  pulp 
nodules  and  calcareous  degeneration  of  the  pulp. 

Tubular  Calcification. — Definition. — By  tubular  calcification,  or, 
to  express  the  condition  more  accurately,  tubular  dentinification,  is 
meant  the  change  that  occurs  in  the  dentin  which  leads  to  an  obliter- 
ation of  the  dentinal  tubuli  by  deposition  of  dentinal  material  along 
the  inside  of  the  w^alls  of  the  tubules,  with  a  corresponding  atrophy 
of  the  fibrils.    It  is  a  sclerosis  of  dentin  analogous  to  osteosclerosis. 

Causes  and  Occurrence. — The  apparent  cause  is  a  mild  degree  of 
irritation,  not  passing  the  stage  inducing  constructive  metamorphosis, 
and  apparently  caused  by  direct  irritation  of  the  fibrils,  more  par- 
ticularly through  the  action  of  thermal  shock,  brushing,  mastication, 
29 


450       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

or  action  of  acids.  It  occurs  in  the  course  of  mechanical  abrasion 
and  erosion  of  the  teeth,  under  metalUc  fiUings,  and  probably  a 
modification  of  the  process  precedes  the  slow  invasion  of  dental 
caries.  It  begins  at  once  the  enamel  is  removed  from  the  dentin  at 
any  point,  and  the  dentin  subjected  to  irritation,  showing  it  to  be 
due  to  a  stimulation  of  the  whole  odontoblastic  cell  (including  its 
fibrillar  prolongation).  It  occurs  in  some  degree  as  a  normal  vital 
change  due  to  age,  and  is  common  in  persons  who  are  victims  of  the 
gouty  or  rheumatic  diathesis.  It  also  occurs  in  pyorrhetic  teeth  as 
a  result  of  pulp  stimulation  (Figs.  304,  353,  c,  and  397). 

Pathology. — The  fibril  is  lessened  in  diameter  as  the  lumen  of  the 
tubule  becomes  smaller.  There  is  sometimes  an  increased,  but  more 
often  a  lessened,  sensitivity  of  the  dentin. 

Other  phases  of  the  condition  are  discussed  under  transparency  of 
the  dentin,  to  which  the  disease  corresponds.    (See  p.  380.) 

The  altered  dentin  becomes  translucent,  acquiring  a  horn-like 
appearance,  and,  usually,  secondary  dentin  formation  begins  coinci- 
dently  with  it.  Andrews  claims  that  granules  of  calcific  matter  are 
pushed  into  the  fibrillse  by  the  odontoblasts  and  deposited  along  the 
inner  wall  of  the  tubule,  even  to  obliteration  of  them.  These  gran- 
ules give  the  color  to  abraded  dentin  in  the  region  of  the  pulp  cavity. 

Tubular  calcification  is,  for  the  most  part,  to  be  regarded  in  the 
light  of  an  effect  due  to  a  physiological  process.  It  may  be  regarded  as 
a  physiological  barrier  erected  against  the  progress  of  caries,  erosion, 
or  abrasion,  threatening  the  invasion  of  the  pulp.  While  it  delays 
the  disintegration  of  the  tissue,  it  does  not  prevent  it.  In  the  cases 
due  to  age  or  the  irritants  produced  by  goutiness,  it  is  probably 
a  local  expression  of  a  general  sclerotic  change,  the  intercellular 
substance  (tubule  wall)  being  formed  at  the  expense  of  the  cellular 
(fibrilla).  In  senility  the  change  in  the  dentin  may  cause  the  teeth 
to  be  almost  transparent.    It  requires  no  treatment. 

Secondary  Dentin. — Definition. — ^By  secondary  dentin  is  meant  a 
deposit  of  dentin  upon  the  wall  of  the  pulp  chamber,  as  the  result 
of  pulp  stimulation  after  the  pulp  has  enjoyed  a  physiological  period 
of  rest  from  dentin  formation.    It  is  always  attached  to  the  dentin. 

Causes. — The  cause  of  formation  of  secondary  dentin  is  a  stimula- 
tion of  the  pulp  to  increased  functional  activity.  This  stimulus 
may  be  provided  by  any  constant  irritation  of  the  dentinal  fibrils, 
as,  for  example,  when  exposed  at  necks  of  teeth,  upon  abraded  or 
eroded  surfaces,  or  within  cavities  of  decay.  The  presence  of  metallic 
fillings,  conductive  of  thermal  changes,  may  provide  the  necessary 
stimulus.  Gold  crowns  upon  ground-down  crowns  of  vital  teeth  have 
a  similar  effect.     The  slightly  irritative  effects  of  oxychlorid  of  zinc 


SECONDARY  DENTIN 


451 


often  produce  much  secondary  dentin.  It  is  associated  with  tubular 
calcification.  A  pulp  capping  may  provide  the  stimulus  and  new 
dentin  fill  the  orifice  of  exposure.    Absolute  exposure  without  treat- 


FiG.  390 


Fig.  392 


Secondary  dentin 
formed  after  exposure 
of  pulp  by  fracture 
during  extraction. 

(Tomes.) 

Fig.  391 


Bicuspid  in  which  a 
formation  of  second- 
ary dentin  has  failed 
to  obviate  perforation 
of  the  pulp  cavity  by 
resorption.       (Tomes.) 


Harding's  case  of  united  fracture.  The  uniting  material 
is  of  coarse  osseous  structure  with  numerous  lacunal  spaces. 
(Tomes.) 


ment  has  been  recorded  as  productive  of  sec-  ^^°-  ^93 

ondary  dentin.  In  two  cases  described  by 
Charles  Tomes,  pulps  widely  exposed  by  frac- 
ture of  crowns  during  extraction  covered  them- 
selves completely  in.  The  histological  record, 
as  seen  in  the  photomicrograph,  demonstrated 
that  a  plastic  exudate  was  first  exuded,  which 
later  calcified  as  an  amorphous  mass. 

Next  an  irregular  lamina  was  formed,  and 
lastly,  dentin  containing  tubules.  It  is  to  be 
inferred  that  both  the  pulp  and  its  odonto- 
blasts may  take  part  in  the  process  (Fig. 
390). 

I  have  seen  one  case  in  which  a  wide  exposure  had  been  covered  in 
sufficiently  to  enable  me  to  gently  indent  the  covering,  which  was 


Elastic  layer  of 
calcific  material  formed 
over  an  exposed  pulp. 
(From  a  case.) 


452       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

convex,  with  a  ball  burnisher.  Upon  removal  of  the  instrument  it 
resumed  its  original  shape,  owing  to  its  elasticity.  The  periphery  of 
the  original  exposure  was  clearly  defined  (Fig.  393).  In  another  case 
of  known  exposure  with  bleeding  the  patient  kept  eugenol  on  cotton 
in  the  cavity.  After  several  weeks  the  exposure  could  not  be  again 
discovered.  Age  seems  to  be  a  cause  of  general  secondary  dentin 
formation,  but  no  doubt  certain  forms  of  irritation  are  introduced 


Fig.  394 


Fig.  394. — Secondary  dentin  filling  the  pulp  chamber  is  a  case  of  abrasion  of  a 
cuspid  tooth:  a,  portion  lost  by  abrasion;  c,  abraded  surface;  d,  secondary  dentin, 
filling  a  portion  of  the  pulp  chamber,  and  acting  as  a  protection  to  the  pulp ;  e,  slender 
point  of  the  pulp — irregular  deposits  are  seen  on  the  walls  of  the  pulp  chamber,  as  at 
/;  g,  cylindrical  calcifications  in  the  root  portion  of  the  pulp  chamber. 

Fig.  395. — Secondary  dentin  from  the  same  specimen  as  Fig.  394,  magnified  suffi- 
ciently to  show  the  difference  in  primary  and  secondary  tissue:  a,  abraded  surface 
crown;  b,  secondary  dentin;  c,  primary  dentin;  d,  junction  of  primary  with  secondary 
dentin;  e,  remains  of  pulp  tissue;  /,  small  oval  masses  of  calcific  material.     (Black.) 


competent  to  produce  the  changes;  for  example,  slight  looseness  of 
teeth,  causing  a  constant  pulp  stimulation.  At  times  reflex  irrita- 
tion seems  to  be  a  competent  cause,  as  in  cases  of  partial  abrasion 
the  unworn  teeth  may  be  affected  in  equal  degree  with  the  worn 


ones. 


It  is  also  true  that  any  form  of  chronic  irritation  of  the  pericemen- 
tum of  a  tooth  may  produce  arterial  hyperemia  of  a  pulp  which  will 
lead  to  the  formation  of  secondary  dentin  or  pulp  nodule  or  both. 


SECONDARY  DENTIN 


453 


Non-occlusion,  mal-occlusion,  pyorrhea  alveolaris  are  typical  ex- 
amples of  the  non-septic  and  septic  classes  of  irritation.  (See  p.  469). 
Pathology  and  Morbid  Anatomy. — The  formation  is  usually  noted 
opposite  to  some  area  of  injury,  and  may  be  distinguished  from 
normal  dentin  by  its  translucency,  or  sometimes  by  its  color,  which 
may  be  a  light  brown.  The  deposit  may  be  of  fairly  regular  or 
irregular  distribution,  and  even  tumors  attached  to  the  dentin  have 
been  described  (Fig.  396). 

Fig.  396 


Dentinal  tumor  within  pulp  chamber:  A,  diagram  of  the  tooth,  with  dotted  line 
showing  the  position  of  the  section  B.  In  B  the  pulp  chamber  is  shown  in  section, 
nearly  natural  size,  showing  the  tumor  within.  C  is  an  illustration  of  the  tissue  of  the 
tumor;  a,  a,  the  primary  dentin;  b,  irregular  tubules  connecting  the  newgrowth  with 
the  primary  dentin — most  of  these  are  very  dark  and  irregular;  c,  c,  a  calcospherite 
included  in  the  mass;  d,  apparently  a  bloodvessel  calcified;  e,  calcified  tissue;  /,  a 
finely  granular  mass;  g,  a  spur  of  very  transparent  dentin.  Dentinal  tubules  appear 
at  h,  h.     (Black.) 


Black  has  shown  that  in  the  deposits  against  normal  dentin  the 
first-formed  portion  contains  an  almost  normal  number  of  tubules, 
but  their  direction  is  sharply  changed.  As  the  deposits  become 
thicker  the  tubules  become  fewer,  and  finally  the  dentin  becomes 
amorphous  in  character  (Fig.  399.) 

Black  relates  these  appearances  with  the  gradual  atrophy  and  dis- 
appearance of  the  odontoblasts.  As  the  pulp  becomes  smaller  it 
also  necessarily  undergoes  atrophy. 


454       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

Hopewell-Smith/  treating  of  secondary  dentin  under  the  title  of 
"Adventitious  Dentin,"  mentions  several  varieties:  (1)  Fibrillar,  or 
that  containing  tube-like  markings  finer  and  less  regular  than  in 
normal  dentin.  This  would  correspond  to  that  in  Fig.  396,  h.  (2) 
Areolar,  that  containing  interglobular  spaces  formed  by  the  non- 
union of  calcospherites.  (3)  Cellular,  in  which  the  cells  of  the 
pulp   remain   encapsulated   in  the   calcifying  matrix.      (Fig.  400.) 

(4)  Laminar,  in  which  laminated  spherites  appear   (Fig.   396,  c). 

(5)  Hyalin,  having  a  granular  or  ground-glass-like  appearance  (the 
amorphous  substance  of  Black)  (Fig.  396,/).  He  regards  the  adven- 
titious dentin  as  formed  by  pulp  cells  rather  than  by  the  odontoblasts. 
In  these  cases  the  pulp  deposits  calcoglobulin  against  the  dentin. 


Fig.  397 


Fig.  398 


Fig.  397. — Illustration  of  the  narrowing  of  the  pulp  chamber  in  a  molar  (superior) 
by  the  deposit  of  secondary  dentin  resulting  from  abrasion,  showing  the  portions  of  the 
chamber  in  which  the  deposit  usually  occurs.  The  light-shaded  portion  (6)  shows  the 
original  dimensions  of  the  chamber,  which,  in  this  instance,  seems  to  have  been  pretty 
large;  a,  a  point  of  deep  abrasion;  c,  c,  remaining  pulp  chamber,  which  is  mostly 
filled  with  irregular  masses;  d,  one  of  the  root  canals.  It  will  be  observed  that  the 
narrowing  of  the  root  canal  is  within  the  original  pulp  chamber.     (Black.) 

Fig.  398.- — P.D.,  primary  dentin;  S.D.,  secondary  dentin;  P,  pulp  chamber;  D,  D, 
nodules. 


Apparently  in  some  of  Black's  cases  the  calcoglobulin  was  deposited 
about  preexisting  fibrillse  which  continued  to  persist  in  the  new 
formation,  the  remaining  odontoblasts  receding,  while  in  Tomes' 
cases  the  pulps  were  compelled  to  calcify  a  plastic  exudate  as  a  sort 
of  basis  for  the  beginning  of  tubule  formation.  This  is  probably  the 
case  in  formation  of  secondary  dentin  as  a  repair  of  exposure  under 
a  cap.  Black  has  shown  that  in  abrasion  the  deposit  is  more  regular 
than  in  caries,  without  doubt  due  to  the  fact  that  the  thermal  irrita- 
tion in  caries  is  more  irregular  than  the  irritation  of  the  fibrillse  by 


1  Histology  and  Patho-Histology  of  the  Teeth. 


SECONDARY  DENTIN  455 

abrasion.  A  deposit  projecting  from  any  point  about  the  pulp  cavity 
side  into  the  pulp  is  called  a  "dentinal  tumor"  (Fig.  396). 

The  entire  crown  may  be  removed  by  abrasion  and  yet  the  pulp 
be  protected.  In  some  cases  the  protective  action  ceases  and  the 
pulp  becomes  closely  approached  or  exposed  (Fig.  280),  probably 
due  to  a  cessation  of  secondary  dentin  formation,  the  result  of 
degeneration  and  loss  of  odontoblasts,  or  it  may  be  due  to  very 
rapid  wear  (a  later  stage  of  Fig.  395). 

The  mode  of  deposition  upon  the  sides  of  the  canal  in  abrasion, 
shown  by  Fig.  394,  is  quite  characteristic,  and  sometimes  annoying 
in  that  it  permits  an  unlooked-for  exposure,  which,  upon  cocain 
anesthesia,  causes  one  to  follow  a  fine  opening  for  an  eighth  of  an 
inch  or  more  before  finding  a  proper  canal. 

Deposits  in  canals  may  occur,  lessening  their  lumen  and  increasing 
the  difficulty  of  canal  exploration  (Fig.  398). 

"Secondary  growths  in  cases  of  abrasion  are  not  confined  alone  to 
the  abraded  teeth,  but  other  teeth  which  have  escaped  wear  may  be 
affected  in  equal  degree.  In  all  of  these  cases  there  is  direct  evidence 
that  the  odontoblastic  layer  has  been  stimulated  to  increased 
activity  and  produced  the  regular  secondary  deposition."^  (See 
Reflex  Hyperemia  of  the  Pulp,  p.  470). 

Secondary  dentin  is  often  accompanied  by  other  constructive 
changes  in  the  pulp — i.  e.,  pulp  nodules  and  calcareous  degeneration 
(Figs.  398  and  404). 

Miller  has  shown  that  dentin  resorption  by  the  pulp  may  be 
repaired  by  a  new  deposit  of  secondary  dentin,  which  Hopewell- 
Smith  has  shown  to  be  of  the  nature  of  cementum.     (Fig.  422.) 

Tomes^  describes  and  illustrates  a  peculiar  case  of  united  fracture 
occurring  in  the  practice  of  Mr.  Harding.  In  an  incisor  an  oblique 
fracture  occurred  which  entirely  separated  the  fractured  segment, 
yet  a  plastic  exudate  occurred  which,  when  calcified,  attached  it  to 
the  fixed  portion  of  the  tooth.  The  new  formation  did  not  resemble 
dentin  (Fig.  392). 

Fig.  309  illustrates  a  case  of  repair  of  an  incisor  fractured  at  a 
point  well  up  beneath  the  gum,  a  condition  reasonably  insuring 
asepsis.  A  firm  reattachment  occurred.  I  have  seen  such  a  fracture 
which  resulted  in  pulp  death  and  the  coronal  portion  remained  in 
situ  for  two  years  (according  to  the  patient).  This  would  give  time 
for  such  a  plastic  exudate  to  form.  In  another  case  I  was  compelled 
to  remove  a  pulp  for  hyperemia  two  months  after  a  fall  fractured  a 
tooth  in  this  location  (see  p.  324). 

'  Black:  American  System  of  Dentistry,  vol.  i.  ^  Dental  Surgery. 


456       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

Kirk^  records  a  case  of  immediate  replantation  in  early  life,  followed 
in  old  age  by  root  resorption.  The  tooth,  when  extracted,  contained 
secondary  dentin,  which  could  only  have  formed  as  the  result  of  a 
reattachment  of  the  pulp. 

W.  H.  Trueman^  reported  that  hypersensitive  dentin  was  noted 
some  years  after  a  replantation  under  similar  conditions. 

Fig.  399 


Calcification  or  deposit  of  secondary  dentin,  resulting  from  caries  of  an  incisor: 
A,  diagram  of  section  of  incisor,  showing  caries  at  a,  and  secondary  dentin  at  b.  B, 
illustration  magnified  200  diameters,  to  show  the  tissue  of  the  secondary  dentin:  a, 
pulp  chamber;  b,  h,  secondary  dentin;  c,  primary  dentin.  It  will  be  noticed  that  the 
dentinal  tubes  in  the  secondary  dentin  gradually  disappear,  giving  place  to  a  clear 
calcification.     (Black.) 

Osteodentin. — Tomes  states  that  secondary  dentinal  deposits  may 
assume  the  character  of  osteodentin,  a  form  of  dentin  found  in  the 
teeth  of  some  animals,  in  which  the  tissue  presents  combined  char- 
acteristics of  both  bone  and  dentin.  He  cites  the  example  also  that 
elephants'  tusks  are  frequently  repaired  with  osteodentin  after  injury. 
The  specimen  illustrated  (Fig.  400)  was  taken  from  a  case  in  which 
the  coronal  portion  of  the  pulp  chamber  was  almost  obliterated  by 
a  deposit  of  secondary  dentin.  Probably  some  of  the  pulp  cells 
have  taken  on  the  characteristics  of  osteoblasts.  Tissue  resembling 
cementum  seems  to  be  frequently  found  as  a  tissue  of  repair  (Fig.  400). 


Proceedings  of  the  Academy  of  Stomatology,  1902. 


2  Ibid. 


SECONDARY  DENTIN 


457 


Results  of  Secondary  Dentin.— The  formation  of  large  masses  of 
secondary  dentin  unquestionably  brings  about  a  degenerative  con- 
dition of  the  pulp  which  may  become  a  cause  of  neuralgia.  The  pulp 
may  die,  and,  becoming  infected,  may  produce  pericemental  irrita- 
tion. In  one  case  seen  the  secondary  deposit  in  the  pulp  chamber 
had  separated  the  canal  filaments  of  the  pulp  of  a  multirooted  tooth 
into  independent  pulps,  one  of  which  was  dead  and  the  others  alive 
and  undergoing  degeneration.  The  specific  symptoms  were  those  of 
pericementitis—?',  e.,  elongation  and  tenderness  to  percussion. 

In  another  case  of  a  first  upper  bicuspid  the  lingual  filament  was 
perfectly  covered  in  and  vital.  The  buccal  filament,  likewise  enclosed 
and  isolated,  contained  an  abscess  within  the  pulp. 

The  symptoms  complained  of,  however,  were  those  of  acute  peri- 
cemental irritation,  simulating  incipient  septic  apical  pericementitis 
(Fig.  432). 

Fig.  400 


Osteodentin:  A,  outline  of  incisor,  showing  a  narrowing  of  the  root  canal  at  b  by 
a  deposit  of  osteodentin.  B,  illustration  of  the  tissue:  a,  primary  dentin;  b,  line  of  the 
beginning  of  a  growth  of  secondary  dentin;  c,  secondary  dentin;  d,  layer  of  granular 
matter-  e,  osteodentin;  this  has  the  lacunaj  at  g  and  dentinal  tubes  at  fc;  /  seems  to  be 
the  surface  of  the  osseous  deposit;  i,  irregular  crystalline  deposits;  h,  the  pulp  chamber. 
X  350.     (Black.).     (Tomes.) 

It  has  been  shown  by  Hopewell-Smith  that  microorganisms  may 
enter  the  pulp  by  way  of  the  spaces  or  tubes  in  adventitious  dentin. 
In  Burchard's  case  a  molar  containing  a  deep  cavity  filled  with  zhic 
phosphate  gave  vague  pain,  finally  referred  to  the  tooth,  which 
responded  only  faintly  to  hot  applications  and  not  at  all  to  cold  ones. 
Secondary  dentin  was  found  complicated  by  calcareous  degeneration 
— i.  e.,  a  degenerated  pulp  was  present. 


458      CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

In  certain  cases  a  deposit  extends  well  into  a  canal,  totally  obliter- 
ating it  for  much  of  its  length.  Unless  symptoms  be  present  it  may 
ordinarily  be  left.  In  such  cases  thermal  tests  for  pulp  vitality  seem 
often  inconclusive.  The  electric  current  should  be  a  more  satisfac- 
tory means  of  diagnosis,  provided  the  dentin  be  moist.  Secondary 
dentin  is  sometimes  quite  hypersensitive,  as  shown  by  attempts  at 
entering  the  pulp;  in  most  cases  it  is  quite  insensitive  until  the  pulp 
is  reached.  It  is  also  difRcult,  as  a  rule,  to  force  cocain  through 
secondary  dentin,  even  with  a  compound  syringe,  and  arsenic  acts 
slowly,  though  it  devitalizes  if  the  dentin  be  sensitive.  (See  Dry 
Gangrene,  p.  562,  also  p.  424.) 

Treatment. — Secondary  dentin  which  has  been  regularly  deposited, 
and  particularly  in  the  canals  of  anterior  teeth,  calls  for  no  treatment. 
Should,  however,  great  hypersensitivity  of  the  dentin  and  pulp,  or 
pulp  disease,  be  evident  or  inferred  from  symptoms,  the  pulp  should 
be  removed.  Canal  opening  may  involve  a  search  of  some  difficulty 
and  necessitate  the  removal  of  much  dentin.  The  canals  may  be 
much  constricted,  especially  at  that  portion  nearest  the  pulp  cham- 
ber. The  condition  may  be  more  or  less  complicated  by  the  presence 
of  pulp  nodules  or  calcific  degenerations  in  addition  to  the  secondary 
dentin. 

Pulp  Nodules. — Definition. — Pulp  nodules  (pulp  stones,  nodular 
calcifications)  are  masses  of  more  or  less  translucent,  calcific  material, 
apparently  the  result  of  secretion,  having  a  fairly  definite  histological 
structure  differing  from  that  of  dentin,  and  occupying  a  position 
within  the  pulp  substance.  They  are  rarely  fused  with  the  dentinal 
walls  of  the  pulp  chamber,  and  then  are  included  by  formation  of 
secondary  dentin  about  them. 

Occurrence. — While  these  growths  may  occupy  the  pulp  chambers 
of  teeth  in  which  the  pulp  has  been  the  seat  of  direct  irritation,  their 
occurrence  is  by  no  means  confined  to  such  teeth.  They  are  found  not 
only  in  teeth  which  have  suffered  abrasion,  erosin,  and  slowly  pro- 
gressing caries,  but,  as  pointed  out  by  Black,  they  may,  and  frequently 
do,  form  in  other  teeth  of  the  same  denture  which  are  not  directly 
involved  in  the  irritation.  This  investigator  notes  that  irritation  of 
the  pulp  of  one  tooth  of  a  denture  very  frequently  causes  a  general 
hyperesthesia  (due  to  mild  reflex  hyperemia)  of  the  pulps  of  all  of 
the  teeth.  Pyorrhea  producing  tooth  movement  or  apical  peri- 
cemental irritation  can  produce  arterial  hyperemia  of  the  pulp  and 
thereby  pulp  nodules.  This  is  due  to  the  constructive  effect  of  mild 
hyperemia. 

Nodules  and  secondary  dentin  or  pulp  hyperemia  may  occur  in 
sound  teeth  ground  for  crowns.     This  simply  indicates  a  necessity 


PULP  NODULES 


459 


for  antisepsis  in  the  cement,  or  a  non-conductor  as  varnish,  or  chloro- 
percha  over  the  teeth  before  cementation.  The  conditions  are  not 
unlike  those  in  a  cavity  of  simple  depth  and  to  the  mind  of  the 
writer  do  not  necessitate  devitalization  before  crowning,  as  many 
live  for  years.    Nodules  are  found  much  more  frequently  in  the  teeth 

Fig.  401 


FN 


A  pulp  nodule  fused  to  the  parietes  of  a  pulp  cavity.  Prepared  by  grinding:  PA'', 
pulp  nodule;  D,  dentin  of  the  tooth.  X  15.  From  section  by  J.  F.  Colyer.  (Hopewell- 
Smith.) 


of  middle-aged  persons  than  in  those  of  youth,  although  they  may 
be  present  as  early  as  the  ninth  year,  as  shown  by  skiagraphy.  They 
occur  more  frequently  multiple  than  single.  Some  of  the  larger 
nodules  are  evidently  formed  by  the  coalescence  of  smaller  ones. 

Pathology  and  Morbid  Anatomy. — The  structure  of  pulp  nodules 
does  not  resemble  that  of  dentin;  they  possess  about  the  same  degree 


460       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

of  translucency  and  hardness  as  secondary  dentin.  Outwardly  they 
may  assume  almost  any  form;  they  range  in  size  from  minute  bodies 
to  a  size  sufficient  to  almost  obliterate  the  pulp  (Figs.  398  and  404). 

Fig.  402 


Section  of  a  pulp  nodule,  showing  many  calcospherites,  as  pointed  out  by  a.  a.   (Black.) 

A  section  of  a  nodule  exhibits  the  presence  of  a  number  of  concen- 
trically laminated  bodies,  recognizable  as  hardened  calcospherites. 
Black  found  them  to  rarely  make  up  any  considerable  portion  of  the 
bulk  of  the  nodule.  The  remainder  of  the  nodule  is  made  up  of 
structureless  material  which  may  contain  a  few  fine  tubes. 


Deposit  of  calcoglobulin  within  the  tisues  of  an  inflamed  pulp.    (Black.) 

He  also  found  deposits  in  the  pulp  which  throw  light  upon  the 
possible  origin  of  nodules  in  some  cases,  and  to  some  extent  upon 
the  conditions  under  which  they  may  be  formed.  In  the  pulp  of 
a  second  molar  of  a  girl,  aged  fifteen  years,  in  which  there  had  been 


PULP  NODULES 


461 


decided  subjective  evidences  of  pulpitis  recurring  at  intervals  for  a 
period  of  two  months,  he  found  a  mass  representing  a  pulp  nodule  in 
its  soft  state.  ''About  one-half  of  the  coronal  portion  of  the  pulp  was 
involved  in  the  inflammation;  lying  a  little  inside  of  the  layer  of 
odontoblasts  were  several  masses  similar  to  Fig.  403,  having  globular 
forms  in  their  mass  or  attached  to  their  margins.  The  globular 
bodies  present  the  laminated  appearance  of  calcospherites."  These 
masses  may  in  all  probability  be  interpreted  as  intermediate  products 
in  the  formation  of  nodules;   they  have  not  yet  become  calcified. 


Calcification  of  the  dental  pulp  At  A  is  shown  the  outline  of  a  lower  molar  with  a 
cavity  at  h.  The  pulp  chanibei  is  much  reduced  m  size  and  filled  with  calcific  material, 
as  shown  in  B.  a,  a,  large  granular  mass  of  calcific  material,  which  is  very  transparent, 
but  finely  granular.  A  very  few  irregular  lines  are  seen  in  the  centre,  which  slightly 
resemble  dentinal  tubes;  h,  an  erratic  growth  of  irregularly  formed  and  unusually 
transparent  dentin;  c,  line  of  the  growth  of  dentin  from  the  floor  of  the  pulp  chamber — 
the  growth  from  other  directions  is  so  perfectly  regular  as  to  leave  no  markings;  d, 
margin  of  the  cavity  of  decay;  e,  a  bundle  of  cylindrical  forms  of  calcific  material 
extending  down  into  the  root  canal.    These  extended  to  the  apex  of  the  root.     (Black.) 


A  small  nodule  may  be  made  up  of  laminated,  structureless 
material,  the  laminae  being  arranged  about  a  central  nucleus,  the 
nature  of  which  is  not  clear,  but  may  possibly  be  calcified  dead  cells 
(Fig.  405). 

The  conditions  of  calcification  of  nodules  are  not  definitely  known. 
Hopewell-Smith  considers  that  they  are  deposited  by  the  pulp  cells  as 
a  secretion  about  themselves,  and  that  the  cells  are  later  obliterated 
or  may  persist  in  situ  (Fig.  406).    He  also  describes  and  illustrates 


462       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

a  case  of  a  nodule  which  had  within  it  a  pulp  cavity  containing 
pulp  tissue. 

Pulp  nodules  occur,  as  a  rule,  in  the  better  grades  of  teeth  which 
show  constructive  tendencies  upon  the  part  of  the  pulp. 

Fig.  405 


A  pulp  nodule  isolated  from  the  pulp.  Shows  its  central  nuclear  formation  and 
its  concentric  lamination.  Prepared  Vjy  grinding.  X  50.  From  collection  of  G.  W. 
Watson.     (Hopewell-Smith.) 


It  is  possible  that  in  these  pulps  the  pulp  cells  under  conditions  of 
irritation  secrete  calcoglobulin,  which  in  part  is  developed  into  spher- 
ites  and  in  part  remains  without  definite  histological  characteristics. 
The  masses  are  probably  calcified  after  their  deposition.  Whatever 
the  origin  of  the  masses — by  cell  secretion  or  otherwise — the  histo- 
logical record  indicates  a  gradual  increase  in  the  size  of  the  deposit. 
Pressure  upon  the  nerves  results  in  irritation  and  an  increase  in 
pulp  hyperemia  which  causes  the  reaction  to  thermal  changes.  Pulp 
nodules  are  usually  found  in  the  coronal  portion  of  the  pulp,  but 
sometimes  exist  in  the  root  portions,  either  free  or  embedded  in 
secondary  dentin.  If  they  obstruct  the  lumen  of  the  canal  they 
cause  interference  with  the  circulation  and  nerve  tissue  and  may 
produce  great  pain.  Bunting  calls  attention  to  the  possibility  that 
the  nodule  moving  freely  in  the  pulp  may  allow  arterial  pressure  to 
raise  it,  permitting  blood  entrance,  while  the  venous  pressure  may 
return  it  to  place  and  prevent  exit  of  blood  thus  inducing  continued 


PULP  NODULES  463 

internal  pressure  in  the  pulp  (a  venous  hyperemia),  thus  causing 
functional  disturbance  and  pain.^  As  in  the  case  of  secondary  dentin, 
nodules  may  be  produced  by  reflex  hyperemia,  as  they  are  quite 
frequently  found  in  teeth  near  to  an  impacted  tooth. 

Symptoms. — Multiple  nodules  may  exist  in  a  dental  pulp  and  give 
rise  to  no  evident  symptoms  whatever,  as  is  shown  by  their  presence 
in  extracted  teeth,  many  of  them  free  from  caries,  and  in  which  there 
was  no  history  of  pain.  On  the  contrary,  the  pulp  of  a  tooth  may 
react  persistently  to  thermal  changes  or  even  be  the  seat  of  intract- 
able pain  without  a  depth  of  carious  invasion  which  would  lead  to 
the  inference  of  acute  pulp  disease;  and  relief  only  be  secured 
through  devitalization  of  the  pulp,  which  upon  examination  may 
reveal  a  small  or  large  pulp  nodule. 

Fig.  406 


--"*^  MN 


7^v 


MN 


The  formation  of  the  pulp  nodule.  Prepared  by  Mr.  Hopewell-Smith's  process. 
PN,  pulp  nodules;  MN,  meduUated  nerve  bundles;  T,  pulp  tissue;  C,  capillary. 
X  230.     (Hopewell-Smith.) 

The  symptoms  attendant  upon  the  presence  of  nodules,  so  far  as 
they  can  be  made  out,  appear  to  be  of  two  types — those  associated 
with  small  and  those  with  extensive  deposits.  Reflex  pain  is  the 
common  associate  of  both. 

Small  Deposits. — While  it  is  true  that  pulp  nodules  may  some- 
times exist  in  apparently  sound  teeth  without  inducing  pain,  yet  the 

>  Dental  Cosmos,  February,  1912,  p.  169. 


464       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

pulps  of  teeth  containing  them  become  excessively  hyperesthetic 
under  what  are  ordinarily  mild  sources  of  irritation.  This  is  mani- 
fested, first,  through  the  contents  of  the  dentinal  tubuli;  the  dentin 
becomes  exquisitely  sensitive  and  cool  water  directed  into  a  shallow 
cavity  produces  a  paroxysmal  and  excruciatingly  painful  response 
from  the  pulp.  In  the  absence  of  direct,  extraneous  irritation  of  the 
pulp,  the  dental  symptoms  may  be  absent,  but  a  persistent  neuralgia 
may  be  located  at  some  distant  point.  Pain  in  the  ear  is  a  frequent 
symptom.  Occasionally  an  obstinate  scalp  neuralgia,  with  the  exist- 
ence of  a  hyperesthetic  spot,  appears.  Pain  in  the  eye,  with  tender- 
ness over  the  supra-orbital  foramen,  is  also  common.  Guilford^  has 
reported  a  case  of  tic  douloureux  of  two  years'  standing,  the  result 
of  pulp  nodules.  The  pain  may  be  recurrent  or  persistent.  If,  in  the 
absence  of  a  more  probable  explanation  of  the  pain,  the  pulp  nodule  be 


Fig.  407 


Fig.  408 


Fig.  409 


Pulp  nodules  in  the  radicular  and 
coronal  portions  of  the  canal.  (Skia- 
graphs by  Price. 2) 


First  and  second  bicuspid  roots 
filled.  Pulp  nodule  in  first  molar. 
(Skiagraph  by  Lodge.) 


suspected,  and  arsenical  applications  be  made  to  devitalize  the  pulp, 
it  is  found  that  not  only  is  intense  pain  caused,  but  examination  after 
even  a  week  or  more  shows  the  pulp  to  be  still  vital  and  hypersensi- 
tive; and,  in  order  to  eft'ect  its  destruction,  repeated  applications 
and  large  doses  of  arsenic  must  be  used.  Cocain  introduced  by 
cataphoresis  is  also  apt  to  be  slow  in  action. 

Large  Deposits. — In  extensive  deposits  of  pulp  nodules  the 
dentin  may  be  almost  devoid  of  sensation,  and  applications  of  heat 
or  cold,  even  in  large  cavities,  may  be  followed  by  delayed  and  faint 
pulp  response.  Such  cases,  however,  commonly  give  a  history  of 
reflex  neuralgia  and  vague  dental  pains  extending  over  a  period,  it 
may  be,  of  years.    With  some  large  deposit  the  pain  may  be  exquisite. 

Diagnosis. — Their  diagnosis  by  means  of  the  x-rays  is  positive 
(Figs.  407,  408,  and  409),  but  their  diagnosis  by  symptoms  may  only 


1  Private  Communication. 


Items  of  Interest,  1901. 


CALCIFIC  DEGENERATION  OF  THE  PULP  465 

be  inferential  and  confirmation  be  lacking  until  after  devitalization 
of  the  pulp  and  the  finding  of  the  pulp  nodules  in  its  substance. 

The  tardy  action  of  arsenic  is  also  observed  in  the  cases  of  large 
deposit,  it  being  frequently  necessary  to  devitalize  the  pulp  piece- 
meal, and  sometimes  the  arsenic  will  hardly  be  tolerated  at  all. 

Treatment. — Pulps  inferred  or  shown  by  a:-rays  to  contain  nodules 
should  be  removed.  The  cataphoric  apparatus  or  compound  sj'^ringe 
or  even  ordinary  cocain  pressure  may  be  used  to  benumb  the  pulp 
by  cocain;  at  least,  sufficiently  for  the  removal  of  the  nodule.  If 
desired,  the  remainder  of  the  pulp  may  generally  but  not  always  be 
anesthetized  by  the  same  means  and  removed.  The  bloodletting 
attendant  upon  removal  of  the  bulb  of  the  pulp  usually  permits  an 
arsenical  application  for  devitalization  of  the  remainder  of  the  pulp 
to  be  painlessly  made,  but  this  is  not  always  the  case. 

The  same  result  may  be  attained  by  drilling  open  the  pulp  cavity 
while  the  patient  is  under  the  influence  of  nitrous  oxid  gas  or  somno- 
form,  or,  possibly,  intra-alveolar  injection  of  cocain. 

At  times  arsenic  may  be  applied  to  the  pulpal  wall  of  the  cavity, 
if  one  exist,  or  in  a  specially  prepared  pocket,  without  production 
of  painful  reaction. 

After  forty-eight  hours  a  portion  of  dentin  is  to  be  removed  and 
a  stronger  application  made.  When  the  pulp  is  closely  approached, 
the  arsenic  is  to  be  left  a  week  or  longer  in  position,  when,  as  a  rule, 
the  nodule  may  be  removed.  Another  application  may  then  be  left 
in  position  for  a  w^eek  or  longer  to  insure  devitalization. 

If,  after  devitalization,  the  nodule  or  calcific  degeneration  be 
found  as  a  spicular  deposit  in  the  mouth  of  the  canal,  it  may  usually 
be  removed  by  teasing  it  from  side  to  side,  first  soaking  the  part 
with  a  sodium  dioxid  solution,  or  50  per  cent,  sulphuric  acid,  which 
quickly  destroys  the  organic  matter  of  the  pulp. 

Pericemental  reactions  are  quite  apt  to  follow  the  removal  of  such 
pulps.  This  result  is  -best  obviated  by  awaiting  the  thorough  death 
of  the  pulp  filaments  before  attempting  their  removal. 

If  such  reaction  arise,  strong  sedatives,  such  as  menthol  solutions, 
are  to  be  applied  on  cotton  as  root-canal  dressings,  and  counter- 
irritants  are  to  be  applied  to  the  gum.  (See  Non-septic  Apical  Peri- 
cementitis.) 

Calcific  Degeneration  of  the  Pulp. — By  calcific  degeneration  is 
meant  the  infiltration  of  inorganic  matter  derived  from  the  lymph 
into  tissue  which  is  dead  or  undergoing  degeneration.  It  occurs  in 
any  part  of  the  body  in  which  the  necessary  conditions  are  present. 
(See  p.  87.) 

Cause  and  Pathology. — The  conditions  apparently  necessary  for 
the  production  of  calcific  degeneration  are  those  which  occur  in  a 
30 


466       CONSTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

semistagnant  blood  current.  An  acid  reaction  occurs  owing  to  the 
presence  of  an  excess  of  carbon  dioxid,  which  favors  deposition  of 
inorganic  matter.  The  albuminous  matter  of  the  tissue  undergoes 
degenerative  changes  owing  to  the  faulty  nutritive  supply  and  waste 
removal. 

Probably  some  cells  die.  They  or  their  constituents  have  some 
affinity  for  inorganic  salts  which  are  taken  up  from  the  lymph.  Thus 
gradually  the  tissue  becomes  infiltrated. 

Those  causes  which  produce  a  sufficient  degeneration  of  pulp  tissue 
to  induce  the  above  process  are:  (1)  The  pulp  exhaustion  due  to 
the  formation  of  secondary  dentin  or  pulp  nodules;  (2)  continued 
hyperemia  or  chronic  inflammation  in  which  venous  hyperemia  plays 
a  part. 

Fig.  410 


A,  outline  of  a  lower  molar,  with  a  large  carious  cavity  at  a;  b,  pulp  chamber; 
the  shaded  portion,  c,  was  occupied  by  cylindrical  calcifications.  B,  cylindrical 
calcifications.      X  100.     (Black.) 


Pathology  and  Morbid  Anatomy. — The  calcific  material,  unlike  the 
cases  of  nodular  calcification,  encloses  the  anatomical  elements  of  a 
pulp  in  process  of  degeneration  in  a  mass  produced  by  deposition, 
not  secretion.  In  the  root  portions  of  pulps  in  which  fibrous  ele- 
ments have  become  pronounced  the  calcification  may  be  tubular  or 
cylindrical  in  character,  the  nature  of  the  calcareous  masses  being 
apparently  a  deposition  about  and  along  the  fibers  (Fig.  410). 

The  pulps  are,  of  course,  living.  There  is  a  comparative  absence 
of  cellular  elements  in  the  pulp — i.  e.,  they  have  atrophied,  degen- 
erated, and  been  absorbed.  Upon  optical  examination  the  masses 
are  seen  to  be  opaque,  are  brittle,  and  decidedly  unlike  pulp  nodules 
in  form. 

Another  evidence  of  the  cellular  degeneration  is  seen  in  the  great 
ease  with  which  such  pulps  are  removed  after  devitalization,  even 
the  most  minute  apical  portions  freely  coming  away  after  slightly 
catching    a    hook    in    the    pulp — i,    e.,    the    usual    odontoblastic 


CALCIFIC  DEGENERATION  OF  THE  PULP  467 

attachment  to  the  dentin  is  not  present.  When  extracted  these  pulps 
have  a  granular  feel  to  the  fingers,  and  when  dry  may  be  quite  stiff 
(Fig.  411). 

Symptoms. — Degenerations  of  the  pulp,  as  a  rule,  present  symptoms 
of  reflex  pain,  vaguely  referred  to  other  parts.    The  response  to  hot 
applications  is  usually  greater  than  that  to 
cold  ones,  and  both  are  delayed — i.  e.,  five  ^^^-  '^i^ 

seconds  or  more  may  elapse  before  pain 
follows  a  severe  test  like  the  intensely  cold 
spray  of  ethyl  chlorid  or  a  hot  burnisher  or 
blast  of  hot  air.  At  times  with  an  open 
pulp  chamber  the  symptoms  of  chronic 
pulp  inflammation  are  obtained.  There 
may  be  a  painful  reaction  to  arsenic  applied 

to  the  pulp.  ,  Lingual  filament  of  pulp 

^      ^  of  an  upper  molar,  broken 

Diagnosis  and  Treatment. — The  .r-rays  may  in  extraction.  The  rigidity 
afford  a  positive  diagnosis,  but  in  their  ab-     ^^  ^^e  filament  was  due  to 

^     .  .       "  '  1       •    p  *'^®    presence     oi     calcmc 

sence  the  diagnosis,  apart  from  the  mference     granules. 

from  the  symptoms,  is  a  postmortem  one. 

In  cases  warranting  the  interference,  in  which  there  is  a  delayed 

response  to  intense    thermal  tests   applied   to  a   filling  or   a   clean 

pulpal  wall,  the  dentin  over  the  pulp  should  be  removed  and  the 

pulp  devitalized.     Upon  removal  of  the  pulp  it  may  be  found  to 

contain  one  or  more  large  or  many  granular  masses. 

Fig.  411  illustrates  a  case  discovered  upon  fracture  of  a  molar 
during  the  operation  of  extraction.  .  In  another  case  the  pulp  was 
slightly  bendable  when  extracted,  but  after  drying  for  a  half-hour 
became  at  its  apical  end  of  needle-like  sharpness  and  stift'ness.  It 
was  filled  with  calcific  granules. 

The  constructive  diseases  of  the  pulp  are  an  evidence  of  an  attempt 
upon  the  part  of  the  pulp  to  protect  itself;  but  with  the  exception, 
perhaps,  of  a  very  regularly  deposited  secondary  dentin  the  effects 
react  upon  the  pulp  itself,  causing  its  destruction.  To  what  extent, 
therefore,  secondary  dentin  is  beneficial  is  an  open  question. 

Evidences  of  constructive  action  upon  the  part  of  the  pulp  may 
occasionally  be  noted  in  the  temporary  teeth — e.  g.,  secondary  dentin 
following  deep  abrasion. 

There  do  not  seem  to  be  any  observations  as  to  the  formation  of 
nodules  or  calcific  degenerations  in  the  pulps  of  temporary  teeth,  but 
there  is  no  good  reason  why  they  should  not  occur,  particularly  after 
abrasion.  The  pulp  diseases  of  the  temporary  teeth  are  usually  of 
an  acutely  destructive  nature,  which  may  account  in  some  degree 
for  the  absence  of  reports  touching  this  subject. 


CHAPTER  XVI. 

DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP. 

This  class  of  pulp  diseases  consists  of  those  of  an  acute  character, 
although  chronic  diseases  may  arise  as  sequels  of  the  original  con- 
ditions. They  are  essentially  destructive  in  character  and  attended 
by  prompt  degeneration  of  pulp  tissues.  The  most  important, 
clinically,  are  those  having  an  evident  association  with  disorders 
of  the  bloodvessels  of  the  pulp. 

HYPEREMIA    OF   THE   PULP. 

Hyperemia  of  the  pulp  is  an  excess  of  blood  in  the  more  or  less 
dilated  vessels  of  that  organ.  It  is  of  two  forms:  active  or  arterial 
hyperemia,  and  venous  or  passive  hyperemia  or  congestion.  These 
two  classes  differ  in  their  probable  direct  causations  and  in  effects. 

Arterial  Hyperemia  of  the  Pulp. — Definition. — ^Active  or  arterial 
hyperemia  of  the  pulp  is  an  excess  of  blood  in  the  dilated  arteries 
and  capillaries  of  the  pulp,  the  pulp  functions  being  increased  in 
mild  continued  cases  or  disturbed  by  a  gradual  passage  of  the  con- 
dition into  a  venous  hyperemia  in  more  severe  cases. 

Direct  Causes  ( Thermal  Shock) . — The  most  common  cause  of  active 
hyperemia  of  the  pulp  is  a  lessening  of  the  non-conducting  covering 
of  the  organ,  enamel,  and  dentin,  leading  to  either  (1)  direct  pulp 
shock  through  the  chilling  or  heating  of  dentin  by  thermal  changes, 
or  (2)  by  direct  fibril  irritation  which  through  the  odontoblasts  and 
their  neural  connection  invites,  by  vasomotor  stimulation,  a  flow  of 
blood.  This  increases  the  functions  of  the  pulp  and  therefore  its 
irritability  and  response  either  as  pain  or  as  further  hyperemia  or 
both.  With  a  deep  metal  filling  present  the  first  explanation  serves. 
With  a  shallow  metal  filling  the  second  fits  the  fact  of  slow  onset  of 
hyperemia,  recognizable  by  pain  to  cold.  It  is  surprising  to  what 
an  extent  the  pulp  may  protect  itself  against  thermal  stimuli  by  the 
formation  of  secondary  dentin  and  tubular  calcification.  Thus 
teeth  filled  with  metal  alone  often  produce  a  pulp  hyperemia,  of  which 
the  patient  complains  as  painful  reaction  to  cold,  but  which  passes 
away  in  a  few  weeks.  When  the  cavity  is  of  moderate  depth  the 
bruising  of  fibrils  by  filling  and  the  thermal  shock  to  fibrils  are 
(468) 


HYPEREMIA  OF  THE  PULP 


469 


causes  acting  through  fibril  stimulation.  The  vigorous  use  of  sand- 
paper disks  in  finishing  large  fillings  may  precipitate  an  attack  of 
pulp  hyperemia,  but  only  if  the  pulp  is  in  a  critical  condition.  The 
loss  of  tooth  substance  mentioned  may  occur  either  through  abrasion, 
erosion,  fracture,  or  caries.  The  condition  frequently  occurs  without 
direct  exposure  of  the  dental  pulp,  and  at  times  when  cavities  are 
relatively  shallow.  Even  the  simple  cervical  exposure  of  dentinal 
fibrils  may  cause  it,  but  does  not  often  do  so.      (See  explanation  2.) 


Fig.  412. — A,  Cavity  or  metal  filling  approaching  pulp:  B,  hyperemic  (sometimes 
inflamed)  pulp;  C,  area  of  hyperemia  of  apical  tissue,  due  to  extension  from  the  pulp 
or  possibly  to  back  pressure  of  blood. 

Fig.  413. — A,  Area  of  non-septic  inflammation  of  apical  tissue  due  to  injury  as 
from  a  blow  or  malocclusion;  B,  hyperemia  or  mild  non-septic  inflammation  of  the 
pulp  due  to  overflow  from  the  apical  tissue. 

Fig.  414. — A,  pyorrhea  pocket;  septic  inflammation  at  C;  B,  area  of  lesser  inflam- 
mation (non-septic) ;  D,  hyperemia  of  pulp ;  E,  normal  tissue. 

Fig.  415. — A,  ulcerated  or  necrotic  alveolar  wall  due  to  injury  and  infection;  B, 
inflammation  more  or  less  non-septic  (lesser  inflammation) ;  C,  hyperemia  of  pulp 
due  to  overflow  of  blood  at  B.  An  abscess  on  an  adjoining  root  has  the  same  pathology. 
If  extending  to  the  molar  it  infects  its  pulp  from  the  apex.     (See  pages  on  Areas.) 


Irritation  of  Fibrils  by  Sepsis. — Septic  dentin  beneath  fillings  acts 
as  a  cause  by  constantly  irritating  the  dentinal  fibrils.  The  leaving 
of  septic  dentin  in  a  cavity  and  a  leaking  filling  over  sound  dentin  may 
so  act.  Inclusion  of  saliva  beneath  a  metal  or  gutta-percha  filling, 
and  the  imperceptible  shifting  of  a  filling  during  placement,  are 
causes  of  septic  dentin.  Amalgam  may  so  shift  if  slight  yet  excessive 
force  be  used  in  finishing  at  the  first  sitting.  The  sign  is  the  appear- 
ance and  disappearance  of  moisture  at  a  visible  margin  as  the  filling 
is  moved.  This  is  often  unobserved  unless  one  be  very  thoughtful 
of  its  possibility.  The  cement  beneath  an  ill-fitted  crown  also  ap- 
pears to  become  saturated  with  saliva  or  serum,  and  its  odor  indi- 
cates septic  irritation.  This  is  less  likely  to  occur  under  gutta- 
percha, but  odor  can  be  noted  in  some  such  cases.  This  may  be 
the  real  cause  of  death  of  pulp  in  ground  sound  teeth  and  calls  for 
avoidance  by  the  use  of  thymol  in  the  cement.     Acute  hyperemia 


470         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

may  occur  from  the  presence  of  a  pulp  nodule,  probably  also  a  result 
of  mild  hyperemia  produced  by  some  other  cause. 

Associated  Hyperemia  of  Pericementum. — All  pulp  hyperemias,  if 
intense,  may  extend  into  the  apical  tissue  and  cause  pericemental 
hyperemia  with  symptoms  of  tenderness  to  touch  (Fig.  412). 

Indirect  Causes. — Extension  of  Inflammatory  Area. — Pulp  hyper- 
emia may  also  be  caused  by  injury  or  disease  of  the  apical  tissue  of 
a  tooth  containing  a  vital  pulp.  Malocclusion  from  any  cause, 
overfull  fillings  or  crowns,  a  blow,  or  overmalleting,  or  the  extrusion 
occurring  in  pyorrhea  alveolaris,  is  competent  to  produce  an  apical 
hyperemia  or  inflammation  which  extends  into  the  pulp  (Fig.  413). 
An  abscess  upon  an  adjacent  tooth  may  have  its  area  of  hyperemia 
extend  into  the  apical  tissue  of  the  tooth  adjoining,  thus  producing 
hyperemia  of  the  pulp  (p.  135,  Fig.  415).  A  fairly  deep  pyorrhea 
pocket  may  frequently  act  in  a  similar  manner,  the  inflammation 
extending  as  a  non-septic  one  up  to  the  apical  tissue  (Fig.  414). 

Reflex  Action. — An  intense  hyperemia  in  the  pulp  of  one  tooth 
may,  by  reflex  action,  produce  hyperemia,  with  its  characteristic 
response  to  hot  and  cold  applications,  in  another  tooth.  In  a  typical 
case  an  inflamed  apical  half  of  the  pulp  of  a  third  molar  produced 
a  hyperemia  in  the  pulp  of  the  first  bicuspid  which  subsided  upon 
removal  of  the  cause  in  the  molar.  Any  of  the  causes  exciting  hyper- 
cementosis  (being  causes  of  pericemental  hyperemia)  may  produce 
pulp  hyperemia,  the  apical  constriction  being  an  added  complica- 
tion. An  aphthous  ulcer  upon  the  gum  over  a  tooth  has  produced 
arterial  hyperemia  of  the  pulp  by  reflex  or  by  extension  of  the  area 
of  lesser  inflammation  which  may  in  some  cases  extend  a  half  inch 
or  more.  Also  an  ulcerated  alveolar  process  resulting  from  infected 
alveolus,  or  the  use  of  alveolar  forceps,  or  even  the  regular  healing 
of  an  alveolus  after  extraction,  may  cause  it  in  a  healthy  adjoining 
tooth  by  extension  of  the  area  of  inflammation  or  even  in  a  distant 
tooth  by  reflex.  Also  any  irritation  along  any  branch  of  the  fifth 
nerve  or  any  of  its  terminals  may  reflexly  induce  a  hyperemia  of 
the  pulp  (Fig.  415).  A  common  cold  by  irritating  the  terminals 
of  the  fifth  nerve  has  produced  it,  as  may  a  tumor. 

Unquestionably,  systemic  conditions,  as  malaria,  or  syphilis,  or 
irritation  in  another  part  of  the  body  than  that  supplied  by  the  fifth 
nerve,  as  the  uterus  or  bladder,  may  excite  reflex  pain  in  the  teeth, 
which,  if  repeated,  sooner  or  later  excites  a  hyperemia,  as  in  the  case 
of  scalp  tenderness  from  dental  disease,  and  which  will  probably  be 
temporary.  The  mode  of  hyperemia  production  is  probably  a  dila- 
tation of  bloodvessels  due  to  vasomotor  disturbance  produced  by 
reflex  action. 


HYPEREMIA  OF  THE  PULP  471 

Apart  from  the  hyperemia  occurring  in  inflammation  and  that  due 
to  septic  dentin,  or  a  septic  extradental  inflammation,  it  may  be 
said  that  arterial  and  venous  hyperemia  are  mainly  due  to  non- 
septic  causes,  and  even  in  septic  cases  to  be  mainly  in  itself  aseptic, 
in  so  far  as  the  pulp  is  concerned.  For  this  reason  if  the  cause  can 
be  removed  and  the  pulp  sedated  (when  necessary)  prognosis  for 
pulp  conservation  is  favorable,  certainly  in  mild  cases  in  which  the 
pulp  is  not  directly  exposed  by  caries. 

Idiopathic  Hyperemia. — In  some  cases  with  sound  teeth  no  obvious 
cause  can  be  found,  perhaps  the  case  is  one  due  to  infarctions 
(which  see)  or  pulp  nodule.  The  latter  can  be  located  by  skia- 
graphy.    Lower  incisors  are  especially  prone  to  it. 

Symptoms. — The  symptoms  of  arterial  hyperemia  vary  according 
to  the  degree  of  vascular  disturbance.  So  long  as  a  quick,  sharp 
pain  is  produced  by  contact  with  cold  or  hot  substances,  ceasing 
immediately,  and  only  reappearing  in  response  to  direct  stimuli,  no 
serious  vascular  disturbance  is  inferred;  but  when  paroxysms  of 
sharp  pain,  lasting  from  many  minutes  to  hours,  follow  upon  an 
application  of  cold  to  a  carious  cavity,  an  unbroken  enamel  surface, 
a  filling,  or  an  area  of  erosion  or  abrasion,  a  profound  disturbance  of 
the  vessels  of  the  pulp  is  indicated. 

The  pains,  in  the  absence  of  direct  irritation,  are,  as  a  rule,  but 
vaguely  located.  During  paroxysms  it  is  of  a  lancinating  character, 
and  usually  reflected  to  another  part  than  the  tooth  afi^ected — e.  g., 
a  sound  tooth  at  a  distance,  the  gum  between  or  above  the  teeth,  the 
ear,  the  eye,  the  supra-orbital  region,  the  infra-orbital  region,  the 
scalp,  the  chin,  the  arm,  etc. 

As  a  rule,  when  an  upper  tooth  is  affected,  the  pain  is  located  in 
the  superior  maxillary  division  of  the  fifth  nerve;  if  a  lower,  in  the 
inferior  maxillary  division.  The  pain  varies  in  intensity  from  a  vague 
uneasiness  to  an  acute  neuralgic  attack,  with  tender  spots  over  the 
point  of  emergence  of  the  nerve  tracts,  as  at  the  supra-orbital  and 
infra-orbital  and  mental  foramina.  The  neuralgic  pains  are  not 
always  constant;  they  may  disappear  from  the  second  or  third 
division  of  the  fifth  nerve  and  appear  in  the  first. 

The  proof  of  the  direct  connection  betw^een  the  pulp  pain  and  the 
neuralgia  may,  in  some  cases,  be  clearly  made  out  by  the  thermal 
test.  When  a  jet  of  cool  water  is  directed  against  the  tooth  whose 
pulp  is  affected,  it  may  produce,  in  addition  to  a  local  pain,  an 
aggravation  of  the  neuralgic  pains,  but  one  must  carefully  exclude 
the  extradental  causes  before  diagnosticating  a  necessity  for  inter- 
ference with  the  tooth  tested. 


472         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

Pathology  and  Morbid  Anatomy. — The  one  distinctive  and  charac- 
teristic anatomical  condition  associated  with  active  hyperemia  is  an 
irregular  dilatation  of  the  vessels  of  the  pulp.^  Fig.  416  represents 
a  section  of  the  pulp  of  a  tooth  extracted  during  a  paroxysm  of 
acute  pain — "acute  paroxysms  of  pain  lasting  for  an  hour  or  more 
were  occasionally  occurring  in  consequence  of  very  trivial  changes 
of  temperature;  the  condition  had  existed  for  several  weeks."  In 
some  cases  of  a  similar  character — i.  e.,  presenting  the  same  symp- 
toms, but  extracted  during  an  interval  of  quiet — nothing  remark- 
able is  presented.  The  gradual  enlargement  of  the  veins  indicates 
the  lessening  outlet  at  the  apical  foramen;  or,  in  other  words,  the 
beginning  and  establishment  of  a  venous  hyperemia. 

The  most  rational  explanation  of  the  dilatation  of  the  vessels  is 
that  it  is  an  irregular  paralysis  of  vessel  walls — i.  e.,  of  vasomotor 
nerves.  Whether  the  more  usual  painful  responses  of  the  pulp  to 
thermal  stimuli  are  due  to  the  stimulation  of  vasodilator  fibres, 
which  causes  hyperemia,  is  a  matter  of  doubt,  but  the  pathological 
conditions  noted  in  pronounced  hyperemia  signify  a  paralysis  of 
vasoconstrictor  fibers.  Subjected  to  repeated  overstimulation,  they 
become  inactive  and  the  vessel  walls  yield  to  the  pressure  of  the 
blood  column.  Black's  researches  indicate  that  the  vessel  walls  may 
recover  their  tone  and  the  vasoconstrictor  nerves  their  functional 
activity  after  paralysis.  Certainly,  clinical  experience  shows  that 
in  all  purely  arterial  hyperemias,  or  even  those  associated  with  mild 
venous  hyperemia — for  the  two  may  be  inseparable — in  cases  with 
symptoms,  the  cases  can  be  cured  if  the  causes  can  be  removed. 

When  a  tooth  pulp  responds  to  thermal  stimuli,  especially  to  mod- 
erate heat  or  cold,  hyperemia  is  inferred ;  but  whether  the  case  is  one 
of  pure  arterial  hyperemia,  mild  or  severe,  or  of  venous  hyperemia  or 
of  hyperemia  of  true  inflammation  must  be  decided  by  the  nature 
of  the  cause  acting,  the  physical  condition  of  the  pulp  (whether 
exposed  or  not),  the  length  of  time  continued,  and  the  length  of  par^ 
oxysm  produced.  The  fact  of  hyperemia  and  its  location  are  first 
determined,  next  a  cause  is  sought  and,  if  direct,  is  removed  or  ren- 
dered incapable  of  action  by  treatment  of  the  tooth;  for  example, 
placement  of  sedatives,  intermediates,  etc.,  in  cavity  cases,  either 
without  or  with  filling  removed  (if  previously  placed).  Quiet  ensuing 
and  the  pulp  not  being  exposed,  arterial  hyperemia  due  to  the  appro- 
priate direct  cause  is  diagnosed,  tentatively  at  the  first  sitting — 
positively  after  partial  treatment.  This  also  indicates  the  final 
treatment.     If  no  explanation  of  cause  be  found  in  the  crown  of  the 

1  Black:  American  System  of  Dentistry. 


HYPEREMIA  OF  THE  PULP 


473 


tooth  in  question,  the  various  indirect  causes  or  reflexes  are  looked 
for  and  if  one  be  found  it  is  removed  by  treatment.  If  relief 
ensue  the  tentative  diagnosis  of  hyperemia  by  extension  or  reflex 
in  the  pulp  which  seemed  at  fault  is  confirmed  by  the  therapeutic 
test. 

Fig.  416 
h 


Hyperemia  of  the  dental  pulp,  showing  the  injection  of  the  vessels:  a,  a,  mem- 
brana  eboris,  or  layer  of  odontoblasts;  b,  b,  b,  b,  vessel  distended  with  blood:  c,  c,  c,  c, 
points  from  which  the  blood  has  fallen  in  handling  the  section.      (Black.) 


If  the  case  be  idiopathic  and  demand  relief  the  pulp  should  be 
removed  and  the  diagnosis  of  hyperemia  is  confirmed,  though  the 
cause  may  remain  obscure  if  no  nodule  is  found.  In  cases  of  cavity 
with  pulp  exposure,  with  possible  sepsis  and  inflammation,  or  septic 
cases  with  suppuration,  the  symptoms  noted  under  such  conditions 
are  considered.  In  routine  work  such  pulps  are  said  to  be  inflamed 
and  removed;  they  may  be  conserved  in  special  cases  of  course. 
Any  hyperemia  present  is  incidental  to  the  inflammation. 

The  .T-ray  may  be  of  use  in  clearing  the  diagnosis  in  some  cases; 
for  example,  of  pulp  nodules  or  abscess  on  adjoining  tooth. 

The  grade  of  severity  of  hyperemia  is  determined  by  the  pain 
produced  on  application  of  the  thermal  test. 

The  following  history  of  a  case  offers  a  good  example  of  hyperemia 
(so  diagnosticated).     A  central  was  drilled  lingually  with  a  round 


474        DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

bur,  by  a  dentist  who  mistook  a  vital  tooth  for  the  one  threatening 
an  abscess.  Finding  it  vital  when  the  pulp  was  exposed  at  a  minute 
orifice,  he  filled  with  gold,  evidently  laying  a  cylinder  of  gold  across 
the  exposure.  For  two  years  the  pulp  reacted  to  cold,  the  response 
finally  becoming  so  severe  that  each  effort  at  cleansing  the  teeth 
caused  pain  from  thermal  shock.  As  the  adjoining  tooth  was  without 
a  lingual  pit,  and  the  electric  light  showed  a  deep  filling,  it  was 
removed,  and  the  condition  related  found.  The  attempts  to  remove 
the  pulp  by  cocain  pressure  failed  four  times,  once  after  sedation, 
and  repeated  applications  of  arsenic  were  necessary. 

It  is  to  be  remembered  that  arterial  hyperemia  may  be  of  several 
grades  of  severity,  according  to  the  vascular  disturbance. 

Fig.  417 


Dilated  bloodvessels  from  the  dental  pulp  in  hyperemia,  from  tooth  extracted  during  a 
paroxysm  of  intense  pain.   (Black.) 


The  temperature  of  the  water  used  in  testing  should  not  be  lower 
than  60°  F.,  and  it  should  be  applied  drop  by  drop.  A  normal 
pulp  will  rarely  respond  painfully  to  a  few  drops  of  water  at  the 
temperature  named,  flowed  into  a  cavity;  but  a  hyperemic  pulp  will 
almost  invariably  respond  vigorously.  As  a  rule,  a  current  of  air 
from  a  chip  blower  is  a  test  of  sufficient  severity. 

In  the  absence  of  a  carious  cavity  the  source  of  the  pain  is  to  be 
sought  in  large  fillings,  testing  each  tooth  by  dropping  cool  water  on 
the  filling;  in  cases  of  erosion  or  abrasion  the  test  is  made  upon  the 
exposed  dentin.  The  tooth  which  responds  with  a  quick  paroxysm 
of  intense  pain,  passing  away  slowly,  is  diagnosticated  as  the  seat  of 
pulp  hyperemia. 

In  making  this  test  doubt  may  arise  as  to  which  of  two  adjoining 
teeth  is  at  fault.  A  small  square  of  rubber  dam,  with  a  single  hole 
punched  in  its  centre,  may  be  passed  over  the  tooth  to  be  tested,  thus 


HYPEREMIA  OF  THE  PULP  475 

Isolating  it,  yet  the  water  will  remain  in  the  mouth.  As,  before 
stated,  however,  the  location  of  a  hyperemic  pulp  does  not  always 
mean  the  location  of  the  cause,  which  may  be  exterior  to  the  tooth, 
and  should  be  looked  for  elsewhere  before  interfering  with  the  pulp 
hyperemia. 

The  prognosis  of  arterial  hyperemia  is  favorable  for  pulp  conser- 
vation in  the  indirect  cases  and  in  cases  of  cavities  of  decay  which 
admit  of  cleansing  without  pulp  exposure,  or  in  cases  of  filled  teeth 
if  the  fillings  are  removed,  and  in  which  the  paroxysms  have  not 
been  too  severe  or  too  often  repeated.  Properly  protected  from 
thermal  shocks  the  vessels  may  recover  their  tone.  It  is  also  favor- 
able in  cases  of  light  blows  or  malocclusion,  if  rest  of  the  apical  tissues 
be  secured. 

It  would  be  favorable  in  cases  of  deep  erosions  which  can  be  filled 
wdth  non-conductors;  but  this  condition  is  rarely  seen  in  erosion. 
It  is  favorable  in  fractures  without  exposure  if  caps  can  be  secured 
in  place,  but  is  unfavorable  in  ordinary  abrasions  unless  so  much 
deeper  than  the  general  occlusal  level,  that  filling  can  be  placed,  or 
in  sound  teeth  the  pulps  of  which  are  irritated  without  evident  cause, 
and  in  cases  in  which  filling  removal  would  not  leave  room  for  non- 
conductors. In  cases  of  actual  exposure  of  the  pulp  it  contra-indicates 
attempts  at  conservation,  except  in  the  mildest  varieties  and  most 
favorable  circumstances,  and  then  only  when  conservation  is 
important. 

Treatment. — The  therapeutic  principles  involved  in  the  treatment 
of  this  condition  are  the  removal  of  the  source  of  irritation  and  the 
securing  of  physical  rest.  The  treatment  is  directed  toward  immediate 
relief  of  the  existing  condition  and  the  prevention  of  its  recurrence. 
If  a  carious  cavity  exist,  it  is  to  be  freed  from  debris,  and  the  grosser 
portions  of  the  carious  dentin  are  removed;  the  pulp,  if  unexposed, 
is  to  have  the  layer  of  softened  dentin  covering  it  left  unremoved,  if 
leathery  and  not  disintegrated. 

Sedative  agents  are  imperatively  called  for;  of  those  used  the  most 
effective  being  the  oil  of  cloves,  or  eugenol,  equal  parts  of  oil  of  cloves, 
and  phenol,  equal  parts  of  phenol  and  camphor  (phenol  camphor), 
equal  parts  of  phenol  and  thymol  (thymophen),  a  saturated  solu- 
tion of  thymol  in  alcohol  or  of  menthol  in  chloroform  or  menthol, 
3  parts,  phenol,  1,  part,  or  solutions  of  cocain.  Thymol  or  menthol 
crystals  may  be  added  to  any  of  these.  Dentalone  and  Phenandyne 
and  the  fluid  of  "Jodoformagen"  are  valuable  proprietary  prepara- 
tions. These  agents  are  all  germicides  as  well  as  sedatives,  and, 
therefore,  sterilize  the  dentin  of  cavities  in  which  they  are  sealed. 

They  are  to  be  applied  upon  cotton  used  alone  or  the  first  pledget 


476        DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

may  be  covered  with  cotton  and  a  non-irritating  varnish,  as  inspissated 
tincture  of  benzoin,  or  chloro-percha,  or  a  quick  setting  temporar}^ 
cement  is  used  as  a  covering  or  a  previously  prepared  covering  may  be 
used  (see  arsenical  covering).  In  from  twenty-four  to  forty-eight  hours 
the  tooth  is  placed  under  the  rubber  dam  and  excavated  (if  not  a  case 
of  filling  removal) ;  its  walls  are  varnished,  and  over  the  wall  nearest 
the  pulp  a  disk  of  softened  gutta-percha  is  laid.  Over  this  zinc  phos- 
phate paste  is  flowed.  "  Jodoformagen"  may  be  used  in  place  of  the 
gutta-percha.  A  stiff  mixture  of  eugenol  and  Hubbuck's  zinc  oxid 
is  a  very  valuable  sedative  cement  to  be  placed  against  the  floor 
of  an  excavated  cavity.  It  hardens  in  saliva  and  may  remain  a 
time  as  a  test  and  then  be  in  part  left  as  a  permanent  floor  covering. 
After  lining  with  zinc  phosphate  a  gutta-percha  filling  may  be 
introduced  for  a  few  weeks.  In  a  case  with  some  persistence  zinc 
phosphate  or  gutta-percha  may  be  used  to  complete  the  test  for 
six  months  or  a  year.  In  mild  cases  the  filling  may  be  completed 
at  once.  The  conductivity  of  zinc  phosphate  is  too  high  to  be  used 
as  the  sole  material  over  pulps  which  have  been  the  seat  of  pro- 
nounced hyperemia;  with  varnish  it  is  more  useful. 

It  not  infrequently  happens  that  it  becomes  necessary  to  assist  the 
pulp  arteries  to  recover  their  tone  by  means  of  counterirritants 
applied  to  the  gum  over  the  apex  of  the  root.  This  is  especially  true 
in  cases  of  pulp  capping.  Dental  tincture  of  iodin  (iodin,  5iii; 
alcohol,  §j;  dissolve  by  succussion;')  or  potassium  iodid,  sat.  sol., 
and  zinc  sulphate,  sat.  sol.,  p.  seq.,  with  iodin  crystals  to  complete 
saturation^  is  to  be  applied  in  spots  to  the  gums,  or  a  mixture 
of  equal  parts  of  tincture  of  iodin  and  tincture  of  aconite  may  be 
painted  upon  the  gum.  A  mixture  made  of  two  parts  of  tincture  of 
aconite  and  one  part  of  chloroform  is  recommended  by  Jack,^  to  be 
applied  to  the  cleansed  and  dried  mucous  membrane  by  means  of  a 
pad  of  cottonoid,  one-half  inch  wide  by  three-quarters  of  an  inch 
long.  It  should  be  held  in  place  by  the  finger  for  fifteen  seconds. 
Tincture  of  aconite  upon  cotton,  placed  in  the  rubber  cup-applicator 
of  a  cataphoric  apparatus  and  held  against  the  gum  for  a  half  minute 
while  the  current  of  a  few  cells  is  active,  will  produce  a  circum- 
scribed area  of  irritation  which  may  later  lose  its  epidermis.  This 
amount  of  irritation  is  valuable.  A  capsicum  plaster  may  be  used. 
For  any  case  of  obdurate  pain  systemic  sedation  or  derivation  may 
be  employed.    (See  pp.  124  and  491.) 

If  the  pulp  be  exposed,  it  is  probably  the  part  of  wisdom  to  remove 
it,  though  if  for  any  special  reason  capping  be  demanded,  it  may  be 

1  Flagg.  2  Northrop. 

^  American  Text-book  of  Operative  Dentistry. 


HYPEREMIA  OF  THE  PULP  477 

done.    When  the  hyperemia  is  active  both  cocain  and  arsenic  may 
be  resisted. 

In  cases  of  abrasion  or  erosion  an  obtundent  is  appHed;  an  exca- 
vation having  a  retentive  form  is  made,  which  is  varnished  in  the 
pulp  direction  only  and  filled  with  preferably  a  combination  of 
cement  and  metal;  or  in  abrasion  the  pulp  may  require  removal. 
A  tooth  containing  a  large  metallic  filling  must  have  the  filling 
removed,  and  after  reducing  the  hyperemia  a  non-conducting 
layer  must  be  placed  between  the  pulp  and  the  filling.  The  precau- 
tion should  always  be  taken,  when  the  pulps  of  teeth  in  which 
cavities  have  been  prepared  respond  unduly  to  the  temperature 
test,  to  cover  the  dentinal  walls  with  a  layer  of  non-conducting 
material.  In  the  absence  of  this  precaution  the  constant  overstim- 
ulation of  the  pulp  by  thermal  impulses  conducted  through  the 
metallic  filling  may  at  any  time  result  in  hyperemia.  The  same 
precaution  is  necessary  in  any  very  deep  cavity.  It  is  also  Avell 
to  avoid  fibril  irritation  by  acid  of  cement,  septic  cement,  or  thermal 
shock  when  crowns  are  to  be  used  on  vital  ground  teeth.  This  may 
be  done  by  using  a  thin  varnish  of  gum  damar  in  chloroform  plus 
hydronaphthol  over  the  tooth,  and  by  adding  powdered  thymol  to  the 
cement  and  in  some  cases  by  lining  the  crowns  and  posts  with  chloro- 
percha  (see  end  of  chapter  on  moist  gangrene).  If  mild  hyperemia 
occur  after  filling  with  metal,  it  ordinarily  passes  away  after  a  few 
weeks.  The  fibrillse  at  first  rebel,  then  become  tolerant,  owing  to 
tubular  calcification,  etc.,  see  page  449. 

In  the  cases  due  to  hypersensitive  dentin  the  powerful  coagulants 
silver  nitrate,  formaldehyde,  etc.,  are  to  be  tried.  (See  Hyper- 
sensitive Dentin.) 

In  cases  due  to  apical  irritation  not  only  must  counterirritants 
be  applied  to  the  gum,  but  it  may  be  necessary  to  cap  an  adjacent 
tooth  with  a  rubber  dam  guard  in  order  to  guard  against  the  irri- 
tation of  the  apical  tissue  by  overocclusion.  (See  Acute  Apical 
Abscess,  Fig.  549). 

If  the  hyperemia  is  of  a  gradual  onset  and  due  to  an  overoccluding 
filling  or  crown,  this  is,  of  course,  to  be  reduced  to  normal  occlusion. 
If  due  to  the  overocclusion  induced  by  chronic  pyorrhea,  the  over- 
occluding  tooth  is  to  be  shortened.  If  of  acute  onset,  a  guard  may 
also  be  necessary.  As  illustrating  its  effectiveness  in  combination 
with  removal  of  the  cause,  may  be  cited  a  case  of  an  upper  third  molar 
Math  a  small  pyorrhea  pocket  on  the  mesiolingual  aspect  of  the  root. 
It  overoccluded  one  thirty-second  of  an  inch,  each  bite  producing 
excruciating  local  pain,  with  also  reflex  to  the  ear.  In  twenty-four 
hours'  use  of  the  guard,  the  pocket  having  been  treated,  the  occlusion 


478         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

was  almost  normal,  the  reflex  pain  gone,  and  the  guard  was  removed 
and  the  tooth  brought  to  normal  occlusion.  In  all  cases  of  cause 
external  to  the  tooth  the  cause  alone  is  to  be  treated.  Trichloracetic 
acid,  or  silver  nitrate  in  saturated  aqueous  solution,  may  be  applied 
to  inflamed  bone  or  aphthae;  while  "dry  socket"  or  exposed  and 
ulcerated  alveolus  surface  must  be  treated  as  indicated.  (See  Index.) 
The  patient  is  to  be  directed  to  avoid  the  use  of  very  cold  or  hot 
substances. 

In  idiopathic  hyperemia  the  pulp  usually  requires  devitalization, 
though  counterirritants  may  be  tried. 

The  test  of  success  of  remedial  measures  is  the  gradual  reduction 
of  response  to  slight  variations  in  temperature — i.  e.,  the  pulp  grad- 
ually bears  higher  and  lower  temperatures  until,  approximately, 
a  normal  tolerance  is  established. 

As  shown  by  Jack,  this  varies  for  hot  applications  from  152°  F.  to 
118°  F.,  and  for  cold  ones  from  74°  F.  to  32°  F. 

In  order  to  determine  the  rate  of  tolerance  normal  to  the  individual 
he  suggests  that  sound  lower  incisors  be  isolated  by  the  rubber  dam 
and  tested  by  throwing  upon  them  first  water  at  a  temperature  of 
80°  F.  The  temperature  of  the  water  is  then  gradually  lowered  or 
raised  until  slight  pain  is  produced  by  the  test.  The  point  registered 
by  the  thermometer  will  be  the  normal  limit  of  thermal  tolerance  for 
the  particular  test. 

The  data  gained  are  useful  in  determining  the  progress  of  a  case 
of  hyperemia. 

A  lack  of  success  in  the  reduction  of  the  arterial  hyperemia  is 
evidence  that  the  more  severe  condition  of  venous  hyperemia  has 
supervened,  or  perhaps  an  infection  has  caused  a  true  inflammation. 

When,  after  fair  trial  of  conservative  treatment,  the  pulp  is  per- 
sistently irritable,  it  should  be  removed. 

In  the  devitalization  of  hyperemic  pulps  there  is  often  painful  ' 
reaction  to  any  of  the  means  employed.  Some  of  these  pulps  resist 
cocain  pressure  in  any  form  even  after  sedation;  some  yield  after 
sedation.  Sedation  or  depletion  should  precede  arsenical  applica- 
tions, and  if  at  any  time  arsenic  produce  a  painful  hyperemia  or 
aggravate  one  previously  existing,  it  must  be  removed  and  sedatives 
used  before  its  renewal,  or  it  may  be  applied  at  another  portion  of 
the  tooth  while  sedatives  are  kept  against  the  pulp. 

It  is  evident  that  such  a  grade  of  vascular  excitement  as  exists  in 
cases  of  exposed  dentin  is  quite  capable  of  producing  the  constructive 
diseases  of  the  pulp  described  as  secondary  dentin  and  pulp  nodules. 
On  the  other  hand,  inflammation  of  the  pulp  has  produced  resorption 
of  the  walls  of  the  pulp  chamber. 


HYPEREMIA  OF  THE  PULP  479 

Pulp  Irritation  from  Electric  Action. — It  is  of  quite  common  occur- 
rence that  galvanic  electricity  causes  pulp  irritation.  The  cataphoric 
current  too  long  continued  may  induce  a  hyperirritability  of  the 
pulp  amounting  in  some  cases  to  evidence  of  hyperemia,  which 
may  subside  under  proper  treatment  or  eventuate  in  pulp  death  from 
venous  hyperemia.  The  occasional  connection  of  a  newly  placed  or 
bright  amalgam  filling  with  a  gold  fiUing,  bridge,  plate,  or  clasp, 
through  the  medium  of  saliva  or  food  (which  amounts  practically 
to  the  same  thing),  will,  at  times,  produce  painful  galvanic  shocks  in 
a  vital  tooth.  Dr.  Franz  Trauner^  has  reported  that  such  pain  has 
been  felt  in  devitalized  teeth.  This  is  outside  of  the  editor's  experi- 
ence, and  should  not  occur  in  totally  devitalized  teeth,  as  the  electric 
current  is  a  test  for  pulp  vitality.  The  mouth  mirror,  or  a  fork  or 
pin,  touched  to  a  new  amalgam  filling,  may  also  produce  the  pain, 
but  a  nickelled  steel  instrument  usually  does  not. 

Painful  shock  is  sometimes  produced  by  the  animal  electricity 
discharged  from  the  operator  during  dry,  cold  weather.  It  usually 
occurs  when  the  finger  is  placed  upon  a  metal  filling,  or  the  plugger 
point  is  returned  to  a  metal  filling.  Touching  the  metal  part  of  the 
chair  before  approaching  the  patient  will  obviate  this  disagreeable 
contact. 

Treatment. — With  cataphoresis,  the  mischief  being  accomplished, 
the  case  must  be  treated  as  other  arterial  hyperemias. 

In  the  case  of  shocks  from  the  presence  of  the  two  metals  it  may 
be  ignored  if  slight  and  the  filling  new,  as  it  will  probably  soon  pass 
away.  A  well-set  and  brightly  polished  amalgam  filling  may  be 
tarnished  if  necessary  by  touching  it  with  a  1  per  cent,  solution  of 
silver  nitrate;  or,  if  good  color  be  a  necessity,  the  pulp  of  the  tooth 
may  be  well  insulated  by  means  of  a  gutta-percha  substratum,  or 
the  pulp  may  be  devitalized.  If  the  fillings  be  in  adjoining  teeth, 
they  should  be  contoured  so  as  to  touch  persistently  if  possible.  If 
in  the  same  tooth,  the  fillings  should  be  connected  by  either  amalgam 
or  gold. 

Venous  Hyperemia  of  the  Pulp. — Definition. — By  venous  or  passive 
hyperemia  of  the  pulp  is  meant  a  condition  of  the  pulp  in  which 
the  return  of  the  blood  in  the  pulp  to  the  heart  is  mechanically 
prevented. 

Causes,  Pathology,  and  Morbid  Anatomy. — But  two  causes  seem 
competent  to  produce  such  a  venous  hyperemia.  These  are:  (1)  A 
preexistent  arterial  hyperemia;  (2)  thrombosis  of  vessels  at  the 
apex  of  the  pulp  canal.    The  venous  hyperemia  which  is  the  second 

'  See  Dental  Cosmos,  1903. 


480         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

stage  of  inflammation  is  to  be  remembered,  but  excluded  from  present 
consideration. 

In  arterial  hyperemia  the  excess  of  blood  is  contained  in  enlarged 
capillaries  and  arterial  trunks.  The  enlarged  main  trunks  or  trunk 
at  the  apex  of  the  pulp  must  compress  the  veins,  as  the  apex  of  the 
canal  is  unyielding.  In  proportion  to  the  severity  of  the  arterial 
hyperemia,  therefore,  are  the  emergent  veins  unable  to  remove  the 
blood  collected  in  the  capillaries  and  venules,  which  gradually  enlarge 
into  varicosities  in  consequence. 

It  has  been  shown  by  Hopewell-Smith^  that  thrombosis  of  the 
small  veins  and  capillaries  throughout  the  pulp  may  result  in  rupture 
of  the  arteries,  and  hemorrhagic  extravasations  occur — either  single 
or  multiple.  These  he  terms  hemorrhagic  infarcts,  although  the 
description  given  more  accurately  denotes  a  minute  venous  hyper- 
emia.   (See  Fibroid  Degeneration  of  the  Pulp.) 

Black  has  shown  that  the  diapedesis  of  red  corpuscles,  which  is  a 
characteristic  result  of  engorgement  of  the  veins  in  venous  hyper- 
emia, occurs  in  the  pulp.  Edema,  which  usually  accompanies  venous 
hyperemia  in  other  situations,  cannot  well  occur  in  the  pulp  because 
of  its  unyielding  surroundings  (Fig.  418). 

It  is  possible,  however,  that  fluid  may  exude  into  the  perivascular 
spaces,  compressing  the  cellular  elements.  Black  has  shown  that 
deposits  of  lymph  may  thus  occur  in  pulpitis.  The  intense  conges- 
tion and  distention  of  the  vessel  walls  permit  a  free  diapedesis  of 
red  corpuscles  into  the  pulp  tissue.  Disintegration  of  the  red  cor- 
puscles may  occur  and  the  hemoglobin  matter  of  the  corpuscles  may 
be  diffused  through  the  dentin,  giving  it  a  pink  discoloration  tech- 
nically known  as  "suffusion."  The  infiltrated  dentin  may  then 
become  progressively  discolored  through  the  characteristic  changes 
of  color  noted  in  connection  with  gradually  decomposing  hemoglobin 
— becoming  purplish,  dark  blue,  and  finally  blue  black.  The  color 
may  pass  into  the  yellow  or  brown  coloration  (see  Tomes'  case). 
Cases  have  occurred  of  coronal  suffusion  in  which  the  pulp  vitality 
has  persisted  for  months.  In  some  cases  the  bulbar  portion  alone  may 
be  dead.  Partial  gangrene  and  the  general  darkening  of  the  tooth 
may  be  present  even  in  a  single-rooted  tooth  with  the  pulp  partly 
alive.  This  is  proof  that  collateral  circulation  exists  in  the  pulp. 
In  cases  of  suffusion  even  all  the  root  of  a  molar  may  be  suffused, 
and  pericementitis,  associated  with  such  a  hyperemia,  seems  partic- 
ularly intractable.    The  vasomotor  paralysis  is  extreme. 

Tomes^  records  a  case  of  a  blow  upon  four  upper  incisors,  which 

^  Dental  Cosmos,  1907.  2  Manual  of  Dental  Anatomy. 


HYPEREMIA  OF  THE  PULP 


481 


became  loose  and  painful.  A  few  da^^s  afterward  reddish  spots 
appeared  upon  the  labial  surface,  which  later  became  dark  blue. 
These  disappeared  except  for  a  slightly  yellowish  tint.  Four  years 
later  the  pulps  M^ere  found  vital  and  healthy.  This  rare  case  is  con- 
firmative of  the  previous  statements. 

If  a  tooth  receive  a  blow  of  sufiicient  severity,  its  pulp  may  die 
without  much  evidence  of  pulp  pain.  On  the  other  hand,  if  the 
blow  be  less  severe,  it  may  give  evidence  of  an  arterial  hyperemia, 
gradually  increasing  in  severity. 

FiG.'418 


Section  of  hyperemic  pulp,  showang  aneurysmal  dilatation  of  the  vessels,  extra- 
vasations of  blood,  and  red  blood  disks  escaped  apparently  by  diapedesis:  a,  a,  dilated 
vessels;  6,  b,  b,  extra vasated  blood.  Besides  this,  red  blood  disks  are  plentifully 
distributed  everywhere  in  the  neighborhood  of  the  veins.  The  tooth  was  extracted 
during  a  paroxysm  of  pain.     (Black.) 


In  the  former  case  it  is  probable  that  the  bruising  of  the  apical 
tissue  produces  a  condition  of  thrombosis  at  the  apex  which  involves 
the  pulp  by  shutting  off  both  its  afferent  and  eft'erent  vessels.  A 
stagnation  results,  and  death  from  lack  of  nutrition  occurs.  This  is 
also  termed  "jugulation." 

In  the  latter  case  the  thrombosis  has  not  occurred,  but  an  arterial 
31 


482         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

hyperemia  is  set  up  by  the  overflow  of  blood  from  the  apical  tissue 
into  the  pulp,  and  goes  on  to  venous  hyperemia. 

It  is  quite  probable  that  rapid  death  of  the  pulp  in  pulpitis  is  due 
to  the  associated  venous  hyperemia. 

Kirk^  mentioned  an  interesting  case  of  venous  hyperemia  with 
intense  suffusion  of  all  the  teeth  as  the  result  of  hanging.  In  such  a 
case  there  was  arterial  blood  supplied  to  the  teeth,  but  the  venous 
flow  was  checked. 

Symptoms. — The  symptoms  of  this  condition,  in  the  absence  of 
definite  data,  can  only  be  inferential.  When  the  paroxysms  of  pain 
are  continuous,  instead  of  temporary — that  is,  when  the  pain,  instead 
of  temporarily  subsiding,  maintains  a  constant  intensity  for  hours 
and  does  not  respond  promptly  to  sedative  therapeusis,  and  is  accom- 
panied by  a  sense  of  fulness  rather  than  sharp  agony — a  condition 
of  serious  venous  congestion  is  inferred.  The  case  from  which  Fig. 
418  was  taken  had  been  the  seat  of  intense  paroxysmal  pain  for  some 
hours.  Upon  close  approach  to  such  a  pulp,  blueness  of  the  horn 
instead  of  pinkness  may  sometimes  be  seen. 

Prognosis. — Perfect  recovery  from  this  condition  is  extremely 
doubtful,  so  that  if  the  pulp  be  not  intentionally  devitalized  and 
removed,  it  will  undergo  degenerative  changes.  The  fact  that  pulps 
have  remained  alive  for  years,  after  having  been  the  seat  of  marked 
congestion,  scarcely  warrants  the  attempt  to  save  so  seriously 
crippled  an  organ. 

Treatment. — The  prognosis  being  doubtful,  the  pulp  should  be 
obtunded  and  devitalized.  If  the  pulp  pain  does  not  yield  to  seda- 
tives, it  should  be  gently  exposed  if  the  excavation  does  not  accom- 
plish its  exposure.  An  antiseptic  is  to  be  applied,  and  by  means 
of  a  very  sharp  puncture  probe  the  pulp  is  to  be  delicately  punctured. 
A  free  flow  of  blood  follows,  which  relieves  the  vascular  engorgement. 
When  this  is  accomplished  the  cavity  is  to  be  syringed  out  with 
warm  water,  and  a  pellet  of  cotton  containing  a  saturated  solution 
of  menthol  in  chloroform  may  be  sealed  in  the  cavity,  or  simply 
retained  by  means  of  a  second  peflet  of  cotton  saturated  with  in- 
spissated tincture  of  benzoin  or  chloro-percha.  After  twenty-four 
hours  an  arsenical  application  may  be  made  for  the  purpose  of 
pulp  devitalization,  or  the  pulp  may  be  removed  by  other  means  if 
tolerated.  If  desired,  the  bulb  of  the  pulp  may  be  taken  out  under 
general  anesthesia,  or  the  whole  pulp  under  mucous,  or  conductive 
anesthesia  (see  p.  407),  or,  possibly,  under  cocain  pressure  anesthesia, 
though  intense  hyperemia  counteracts,  as  a  rule. 

1  Private  communication. 


INFLAMMATION  OF  THE  PULP  483 

The  extreme  paralysis  of  the  vessel  walls  is  occasionally  shown  by 
persistent  hemorrhage  after  depletion,  and  which  resists  ordinary 
effort  at  limitation.  In  some  cases  the  intense  pain  may  continue 
as  well.  The  application  to  the  pulp  of  a  mixture  of  powdered 
thymol  and  dried  alum,  equal  parts,  taken  up  on  a  pellet  of  cotton 
moistened  with  a  saturated  solution  of  thymol  in  alcohol,  has  proved 
useful  in  some  cases.  A  general  anodyne  may  be  required  for  relief 
of  the  pain, 

INFLAMMATION   OF   THE   PULP  (PULPITIS). 

Definition. — Pulpitis  is  the  occurrence  of  the  phenomena  of  inflam- 
mation within  the  pulp  tissue.  The  characteristic  emigration  of 
leukocytes  from  the  bloodvessel  into  the  perivascular  tissues  must 
have  occurred. 

Causes. — This  morbid  anatomy  is  usually  found  associated  with 
diseases  of  the  tooth  crown  or  pericemental  tissue  which  admit 
bacteria  to  the  pulp.  At  the  same  time  it  is  quite  probable  that 
a  non-septic  irritant,  such,  for  example,  as  a  partially  absorbed 
extravasation  of  red  corpuscles  or  undue  pressure  of  a  filling  upon  a 
thin  lamina  of  healthy  dentin  overlying  the  pulp,  or  as  has  occurred 
of  a  metal  filling  upon  or  even  extending  into  a  pulp,  or  an  escharotic 
applied  to  the  pulp  may  induce  the  characteristic  pathology  of 
inflammation  which  may  be  non-septic  or  septic  according  to  the 
sterility  at  the  time  of  operation. 

According  to  the  character  of  the  cause,  therefore,  inflammation 
of  the  pulp  may  be  divided  into  simple  and  infective.  It  may  be 
that  a  simple  inflammation  may  become  an  infective  one  owing 
to  the  association  of  bacteria — e.  g.,  the  pressure  of  a  foreign  body 
may  initiate  the  process  and  the  inflamed  pulp  become  a  soil  for  the 
propagation  of  the  bacteria  present. 

The  causes  of  pulpitis  may  be  grouped  under  three  headings : 

1.  Mechanical  or  physical  causes,  which  irritate  by  acting  as 
foreign  bodies,  or  by  pressure. 

2.  Chemical  causes,  which  act  as  irritants  by  either  producing  a 
chemical  destruction  of  pulp  tissue,  or  by  irritation  without  direct 
destruction.  In  the  former  case  the  dead  tissue  acts  as  a  foreign 
body  against  which  the  pulp  reacts  in  an  effort  to  cause  its  exfoliation 
or  absorption. 

3.  Parasitic  or  infective,  which  cause  the  phenomena  of  infective 
inflammation. 

Pulpitis  is  classifled,  according  to  its  extent,  into  partial  and  com- 
plete; according  to  its  duration,  into  acute  and  chronic;  according 


484         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

to  its  infective  character,  into  purulent  and  non-purulent;  and, 
again,  according  to  the  character  of  the  degeneration  which  follows 
upon  the  inflammatory  process.  While  pathologically  these  con- 
ditions may  be  clearly  differentiated  from  one  another,  they  may  be 
reduced  to  more  compact  groupings  according  to  their  clinical  sig- 
nificance. For  example,  acute  pulpitis  is  frequently  infective,  partial, 
and  purulent;  chronic  pulpitis  is  frequently  non-infective,  extensive, 
non-purulent,  and  followed  by  secondary  degenerations.  It  is, 
however,  often  purulent,  and,  of  course,  infective. 

For  the  sake  of  convenience,  pulpitis  will  receive  a  clinical  division 
into  acute  and  chronic. 

Acute  Pulpitis. — By  acute  pulpitis  is  meant  that  form  of  inflam- 
mation of  the  pulp  which  runs  an  active  and  more  or  less  violent 
course  toward  pulp  death,  and  has  associated  with  it  acute  par- 
oxysms of  pain. 

Causes. — The  causes  of  acute  pulpitis  are  direct  and  indirect, 
intrinsic  and  extrinsic;  the  vast  majority  of  cases  being  due  to 
extrinsic  causes.  The  direct  intrinsic  causes  are  hemorrhagic  extra- 
vasations accompanying  venous  congestion,  or  thrombosis  (In- 
farction), pulp  nodules,  and  injury  of  the  vessels  at  the  apex  of  the 
root.  The  direct  extrinsic  causes  are,  perhaps,  invariably  associated 
with  bacterial  invasion,  a  possible  exception  being  the  pressure 
of  filling  material  upon  a  thin  elastic  lamina  of  softened  dentin, 
covering  the  pulp.  The  dental  pulp  is  intolerant  of  the  slightest 
pressure,  and  rebels  vigorously  when  subjected  to  compression. 
Irritating  drugs  may  also  act  as  irritants — e.  g.,  zinc  chlorid.  It  is 
not  necessary  that  the  pulp  should  be  exposed  to  permit  bacterial 
infection,  and  extensive  bacterial  invasion  is  probably  not  necessary 
for  the  production  of  pulpitis.  The  waste  products,  ptomains,  etc., 
of  bacteria  may  find  their  way  to  the  surface  of  the  pulp  via  the 
dentinal  tubuli,  through  a  layer  of  softened  dentin,  and  excite 
inflammation.  It  is  extremely  probable  that  infection  of  the  pulp 
is  an  invariable  consequence  of  its  exposure  by  decay;  but  as  a 
pulp  may  be  exposed  without  subjective  evidences  of  hyperemia  or 
inflammation,  it  follows  that  infection  does  not  necessarily  imply 
inflammation,  though  the  absence  of  acute  symptoms  may  be 
accounted  for  by  the  escape  of  the  effusions  into  the  cavity  of  decay. 
The  presence  of  a  gross  irritant,  such  as  a  mass  of  food  debris, 
vegetable  seeds,  bread  crumbs,  etc.,  in  contact  with  the  pulp  will 
precipitate  an  acute  inflammation  in  which  bacterial  relations  must 
be  taken  into  consideration. 

"The  severity  of  the  inflammation  does  not  appear  to  be  pro- 
portionate to  the  number  of  bacteria  present,  and  in  a  highly  in- 


INFLAMMATION  OF  THE  PULP 


485 


flamed  pulp  we  may  be  able  to  find  but  few  bacteria.  .  .  .  The 
conclusion  seems  to  be  justified  that  the  inflammation  is  due  to 
the  combined  action  of  the  bacteria  and  their  products  (acids, 
ptomains,  etc.)  with  which  the  carious  dentin  becomes  impregnated."^ 
Goadby  has  shown  that  the  Streptococcus  brevis  and  Bacillus 
necrodentalis  may  pass  through  the  tubules  of  even  secondary 
dentin. 

Pulpitis  from  injury  of  the  vessels  at  the  apex  of  the  pulp  must 
be  mentioned.  It  may  occur  in  consequence  of  blows,  biting  upon 
hard  substances,  too  rapid  wedging,  the  rapid  movement  of  teeth 
in  orthodontia,^  and  the  progressive  loosening  of  teeth  in  pyorrhea 
alveolaris.     In  these  cases  the  pericementum  is  primarily  affected 

Fig.  419 


Inflammation  of  dental  pulp:  a,  a,  normal  cells;  6,  b,  b,  b,  inflammatory  elements; 
c,  cells  in  process  of  division  (j^  inch.)     (Black.) 


by  a  non-septic  pericementitis  which  extends  into  the  pulp,  producing 
arterial  hyperemia  as  an  accompaniment,  and  the  teeth  are  tender 
upon  percussion  as  well  as  sensitive  to  thermal  changes.  In  these 
cases  the  pulp  may  have  either  hyperemia  or  non-septic  pulpitis, 
impossible  of  differentiation  unless  the  tooth  be  extracted.  Pain 
in  the  teeth  upon  assuming  the  recumbent  position,  dull,  heavy 
uneasiness  about  the  jaws,  and  inordinate  response  to  thermal 
stimuh,  particularly  to  heat,  point  to  pulpitis.  Bacteria  from  an 
abscess  on  an  adjoining  tooth  or  from  a  pyorrhea  pocket  when 
these  actually  reach  the  apical  region  of  the  tooth  in  question  may 

1  Miller:  Dental  Cosmos,  1894. 

2  Buckley,  through  a  circular  letter  to  orthodontists,  obtained  opinions  that  the 
upper  centrals  and  laterals  are  most  liable  owing  to  the  frequency  of  displacement, 
character  of  movement,  prominence  of  location,  and  the  curve  of  lateral  roots.  Items 
of  Interest,  December,  1910. 


486 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


infect  a  pulp  from  the  apex.  This  will  cause  the  death  of  a  single 
pulp,  but  only  inflammation  in  a  multirooted  pulp.  Infection  by 
way  of  the  blood  stream  is  a  possibility.  The  pressure  of  an  impacted 
tooth  may  also  act  as  a  cause  by  pressing  the  apical  tissue,  or  by 
causing  resorption  of  the  root  (see  p.  292). 

Morbid  Anatomy  and  Pathology. — In  determining  the  existence  of 
pulpitis,  no  matter  what  the  symptoms  which  have  presented  or  the 
condition  as  to  exposure,  etc.,  the  microscopic  examination  of  sections 
of  the  affected  organ  constitutes  the  only  decisive  test;  if  the  changes 
characteristic  of  inflammation  be  absent,  no  matter  what  the  symp- 
toms, pulpitis  did  not  exist.    The  essential  feature  of  the  process  is 

Fig.  420 


Interstitial  pulpitis  with  pulp  nodule  in  situ.      (V.  A.  Latham.) 


emigration  of  the  white  blood  corpuscles  from  the  small  veins  into  the 
intercellular  matrix  of  the  pulp.  At  first  the  inflammatory  elements 
(leukocytes)  are  scattered  through  the  spaces  between  the  pulp  cells 
(Fig.  419) ;  at  a  later  stage  the  territory  is  occupied  by  round  indif- 
ferent cells  alone.  The  inflammation  may  be  widespread,  as  shown 
in  Fig.  420,  or  may  be  localized  to  some  portion  of  the  pulp,  as  one 
horn  of  a  pulp;  Black  noted  also  inflammatory  action  occurring  in 
small  islands  (Fig.  421). 

Swelling  of  the  pulp  (from  exudation)  cannot  occur  unless  there  be 
a  break  in  the  wall  of  the  pulp  chamber  through  which  additional 
space  can  be  gained.    Black  has  recorded  that  "he  found  beneath  the 


INFLAMMATION  OF  THE  PULP  487 

layer  of  odontoblasts  in  the  region  of  an  exposure  an  unmistakable 
deposit  of  inflammatory  lymph.  The  case  had  a  history  of  severe 
toothache  for  two  days,  two  weeks  previously.  The  pulp  exhibited 
evidences  of  previous  extravasations  of  blood  from  hyperemia." 

There  is  evidence  that  the  pulp  may  recover  from  attacks  of 
inflammation,  and  that  resolution  occurs.  In  some  cases,  as  shown 
under  the  head  of  calcareous  degeneration,  the  tissues  may  become 
infiltrated  with  calcic  material.  In  others,  chronic  degenerative 
changes — inflammatory  degeneration — may  supervene. 


Minute  inflammatory  focus  within  the  tissues  of  the  pulp:  a,  a,  arterial  twigs; 
h,  a  nerve  bundle;  c,  collection  of  leukocytes.     (Black.) 

Suppuration  of  the  pulp  is  a  common  accompaniment  of  pulp 
inflammation;  this,  being  necessarily  infective,  will  be  described 
separately. 

GaskelP  has  reported  a  case  where  a  central  incisor  entirely  free 
from  caries  exhibited  on  its  palatal  aspect  a  pinkish  tinge,  which 
increased  in  depth  until  the  enamel  overlying  crushed  in,  revealing 
the  pulp  of  the  tooth  lying  immediately  beneath;  there  had  been  a 
resorption  of  a  large  mass  of  the  dentin  lying  between  the  pulp  and 
the  enamel.  The  pulp  was  removed  and  the  tooth  filled.  No  history 
is  given  as  to  the  condition  of  the  root,  whether  resorption  had 
occurred  there  or  not.  Shortly  after,  the  adjoining  central  incisor 
exhibited  a  like  pink  coloration,  which  increased,  leading  to  the 
inference  that  resorption  was  in  progress  in  this  tooth  also.  At  the 
suggestion  of  E.  C.  Kirk  the  patient  received  continued  doses  of 

1  Proceedings  of  the  Academy  of  Stomatology,  Philadelphia,  1895. 


488 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


arsenic  iodid  and  the  compound  syrup  of  the  hypophosphites,  in  the 
hope  of  inducing  a  general  and  local  constructive  metamorphosis. 
This  treatment  was  followed  by  a  gradual  disappearance  of  the  pink 
coloration,  an  evidence  of  a  redeposition  of  dentin.  In  the  absence 
of  histological  data  it  is  impossible  to  state  just  what  was  the  nature 
of  the  repair  tissue  in  this  particular  case,  but  Miller^  has  shown 
that  the  pulp  may  take  up  a  resorptive  function  and  remove  dentin 
which  may  later  be  redeposited  as  anomalous  tissue.  The  new 
dentin  does  not  contain  tubules,  but  has  the  characteristics  of 
cemental  tissue^  (osteodentin),  or  even  bone  with  Haversian  systems^ 
(Fig,  422).  This  process  has  its  analogue  in  the  tusks  of  elephants 
and  also  in  the  production  of  Howship's  lacunae  in  the  resorption  of 
the  pericementum,  these  lacunae  later  being  filled  up  with  cementum. 

Fig.  422 


Resorption  of  the  walls  of  the  pulp  chamber  and  redeposition  of  new  calcific  matter: 
a,  pulp  chamber;  b,  c,  d,  portions  of  resorption  areas  not  refUled  and  walled  off  by  the 
new  deposit-forming  cavities  occupied  originally  by  the  pulp  tissue.     (Miller.) 

There  have  been  cases  of  inflamed  pulp  in  teeth  decayed  while 
yet  impacted.  In  these  cases  there  is  usually  some  form  of  sinus 
connecting  the  tooth  with  the  mouth. 

Symptoms. — The  early  stage  of  inflammation  is  an  arterial  hyper- 
emia, and  as  the  leukocytes  collect  in  the  venules  a  venous  hyperemia 
is  established.  No  matter  how  far  the  area  of  stasis  extends,  beyond 
it  will  exist  an  area  of  arterial  hyperemia.    Owing  to  the  enclosing 


1  Dental  Cosmos,  August,  IQOl. 

2  Hopewell-Smith :  Histology  and  Pathohistology  of  the  Teeth. 


3  Salter. 


INFLAMMATION  OF  THE  PULP  489 

canal  walls  and  constricted  apex  a  general  venous  hyperemia  may  be 
established  which  causes  the  death  of  the  pulp. 

In  view  of  these  facts  it  is  not  surprising  that  the  symptoms  of 
pulp  inflammation  take  on  somewhat  the  characteristics  of  both 
arterial  and  venous  hyperemia.  The  diapedesis  of  leukocytes  and 
exudation  of  fluid  cause  the  phenomena  of  heavy,  boring  pain  and 
a  feeling  of  internal  pressure. 

The  pulp  may  be  exposed  and  no  symptoms  be  present.  A  sudden 
pressure  of  food  or  toothpick,  suction  upon  the  pulp  or  the  contact 
of  cold  or  hot,  salt,  sweet,  or  acid  substances,  may  excite  an  attack 
of  throbbing  or  lancinating  pain.  This  may  be  localized  in  the  tooth 
or  may  be  reflected  to  other  teeth  or  the  parts  mentioned  under 
hyperemia  (p.  471). 

The  assumption  of  the  recumbent  position  permits  an  increased 
flow  of  blood  into  the  paretic  vessels  of  the  pulp  and  increased  suffer- 
ing results  in  correspondence  with  the  law  that  inflamed  parts  are 
always  more  painful  in  the  dependent  position.  (See  p.  131  and 
201.)  Indeed,  recumbency  is  sufficient  at  times  to  induce  a 
paroxysm  in  a  comparatively  quiet  but  inflamed  pulp.  Under  a 
capping  or  filling  pressing  on  the  pulp  or  thin  dentin  the  pain  may 
begin  as  a  slight  pain  and  gradually  increase  in  intensity,  or  it  may 
respond  as  a  sudden  agony,  beginning  even  some  time  after  the 
operation.  This  may  have  been  know^n  at  the  time  of  operation  or 
been  suspected  later.  In  one  typical  case,  violent  reflexes  occurred 
sometime  after  a  metal  filling  was  introduced  over  sound  dentin. 
The  diagnosis  was  uncertain  but  filling  removal  and  placement  of 
eugenol  and  zinc  oxide  cement  for  a  month,  removed  the  reflexes, 
permanent  filling  was  done  and  after  a  year  no  trouble  exists — diag- 
nosis, pressure  irritation.  In  the  later  stage  of  pulp  inflammation 
the  pain  is  of  a  heavy,  boring,  continuous  character,  the  perice- 
mentum becomes  somewhat  hyperemic,  and  the  tooth  responds  to 
tapping.  In  case  of  a  highly  irritable  pulp,  however,  the  concussion 
of  the  pulp  produced  by  tapping  may  readily  cause  pain. 

In  pulpitis  the  pulp  responds  both  to  heat  and  cold,  but,  as  a  rule, 
more  to  the  former  than  to  the  latter.  There  have  been  many  cases 
of  reflex  neuroses  developed  by  inflamed  pulps,  reflex  pains  in  the  face, 
eye,  ear,  neck,  scalp,  chest,  arm,  heart,  etc.,  as  well  as  functional 
disorders  of  the  eye,  ear,  and  brain.  One  case  of  dementia  prsecox 
was  cured  by  removal  of  a  tooth  with  inflamed  exposed  pulp.^  One 
case  of  sensory  paralysis  of  the  entire  left  side  was  caused  by  inflam- 
mation of  a  portion  of  the  pulp  in  a  right  upper  cuspid  and  marked 

1  Upson:  Dental  Cosmos,  1910,  p.  529. 


490         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

relief  began  in  about  an  hour  after  removal  of  a  covering  dressing 
and  filling.  The  symptoms  of  suppurative  inflammation  may  differ 
somewhat  (see  Abscess  and  Ulceration,  p.  492). 

Diagnosis.— The  diagnosis  is  largely  inferential  and  made  by 
observation  of  the  symptoms  and  conditions  existing.  The  pulp 
may  be  exposed  or  closely  approached  by  caries,  or  the  pulp  may 
be  approximated  by  a  large  filling.  If  there  be  a  leak  about  the 
filling,  a  septic  fluid  or  actual  decay  beneath  the  filling  may  be  the 
exciting  cause.  In  the  absence  of  evident  causes  such  sepsis  is  always 
to  have  consideration,  and,  if  necessary,  the  filling  must  be  removed 
and  tests  applied.  The  more  obscure  causes,  such  as  abscesses  upon 
adjoining  teeth,  infection  from  the  pericemental  tract  in  the  course 
of  pyorrhea,  looseness  of  teeth  or  traumatisms,  are  to  be  carefully 
considered.  If  the  tooth  involved  be  uncertain,  each  tooth  should 
be  placed  under  rubber  dam  and  tested  thoroughly. 

Prognosis. — The  prognosis  is  always  bad  for  the  comfortable 
conservation  of  the  pulp,  and  it  should  be  removed  and  the  canal 
filled. 

Treatment. — The  treatment  of  pulpitis  involves  the  reduction  of 
the  amount  of  blood  in  the  vessels  of  the  pulp,  the  sterilization 
of  the  infected  area,  the  relief  from  the  pain,  and  the  removal  of 
the  pulp.  It  is  usual  to  excavate  the  cavity  of  decay  thoroughly 
enough  to  remove  from  over  the  pulp  decayed  dentin  which  would 
prevent  the  action  of  remedies  or  act  as  an  irritant.  The  cavity  is 
then  washed  and  a  sedative  applied.  (See  p.  475.)  A  creamy  paste 
of  bicarbonate  of  soda  in  carbolic  acid  has  been  recommended.^ 
The  addition  of  a  trifle  of  powdered  alum  to  any  of  the  sedatives 
acts  as  an  astringent  to  the  vessels.  During  the  half  hour  succeeding 
the  application  the  pulp  should  give  some  indication  of  relief.  If 
it  be  somewhat  decided,  a  portion  of  the  remedy  used  should,  if 
possible,  be  sealed  in  the  cavity  for  twenty-four  hours.  The  covering 
may  be  prepared  first  as  for  arsenic.  (See  p.  527.)  If  not  possible 
to  seal  it  in,  it  may  be  covered  with  cotton  saturated  with  a  varnish 
made  by  evaporating  tincture  of  benzoin.  This  varnish  hardens 
like  sandarac  varnish,  but,  unlike  it,  is  not  irritant.  Claims  are 
made  for  alcohol  used  as  for  pressure  anesthesia. 

If  after  the  first  half  hour  no  indication  of  relief  has  been  obtained, 
it  is  well  to  expose  the  pulp  and  to  relieve  the  engorged  vessels  by 
delicately  puncturing  it.  (See  Extirpation  of  Pulp.)  After  exposing 
the  pulp  it  will  perhaps  exude  a  bead  of  pus,  which  makes  the  diag- 
nosis one  of  pulp  suppuration.    After  free  bleeding,  which  may  be 

1  Gerdtzen. 


INFLAMMATION  OF  THE  PULP  491 

encouraged  by  means  of  warm  water,  the  sedatives  will  usually  act. 
It  may  be  necessary  at  times  to  employ  short  general  anesthesia 
(nitrous  oxid  gas,  etc.)  as  a  means  to  obtain  free  bloodletting.    Every- 
thing being  prepared,  the  patient  is  anesthetized  and  the  bulb  of  the 
pulp  cut  out,  or  if  N2O  and  O  anesthesia  can  be  used,  the  entire  pulp 
may  be  taken  out.    At  times  cocain  pressure  anesthesia  is  effective 
at  least  for  the  removal  of  the  bulb  of  the  inflamed  pulp,  and  some- 
times of  the  entire  pulp;  often,  however,  it  causes  too  much  pain. 
When  several  trials  have  been  made,  and  even  the  cotton  forced 
into  the  pulp  tissue  without  complete  anesthesia,  a  pellet  of  devi- 
talizing fibre  may  be  put  into  the  pulp  chamber  with  no  discomfort. 
In  case  of  partial  extirpation,  not  only  is  free  bleeding  induced, 
but  the  diseased  pulp  tissue  is  largely  removed.    When  hemorrhage 
ceases  arsenic  may  be  applied,  or  pressure  anesthesia  attempted. 
If  the  hemorrhage  be  obstinate  the  application  of  powdered  thymol 
and  dried  alum  may  be  used.     (See  Venous  Hyperemia.)     When 
sedatives  are  used  upon  the  pulp,  counterirritants  applied  to  the 
gum  are  aids  of  great  value,  and  are  to  be  used  as  described  under 
Arterial  Hyperemia  (p.  476). 

In  addition  to  these  the  principle  of  depletion  may  be  employed. 
Deep  cuts  may  be  made  with  a  sharp  bistoury  in  the  gum  overlying 
the  root  apex.  The  anastomosis  with  the  vessels  of  the  apical  tissue 
is  expected  to  cause  the  cuts  to  act  as  openings  made  in  veins  leaduig 
from  the  inflamed  pulp.  According  to  Nancrede,  depletion  on  the 
venous  side  of  an  inflamed  area  markedly  reduces  engorgement.  In 
addition  to  these  measures  catharsis  is  a  valuable  means  of  derivation; 
a  tablespoonful  of  sulphate  of  magnesia  is  to  be  dissolved  in  a  goblet 
of  water  and  taken  internally  at  least  a  half  hour  before  a  meal. 

If  the  pain  be  obdurate  and  its  return  feared,  two  \  grain  sulphate 
of  morphin  tablets  may  be  dispensed,  preferably  by  the  operator, 
to  be  taken  only  in  case  of  severe  pain  and  an  hour  apart. 
Acetanilid  and  phenacetin  are  also  useful. 

The  following  is  a  useful  anodyne  and  antineuralgic  prescription: 

I^ — Acetphenetidini  (phenacetin) , 

Acetanilidi aa  gr.  xxx 

QuininEe  sulphatis gr.  xv— M. 

Pone  in  capsulas  no.  vi. 

S. — One  morning  and  evening. 

(See  also  Treatment  of  Facial  Neuralgia.) 

HalP  has  suggested : 

R — ^Aspirin 3s3 

Codein g'^-iss 

M.  et.  ft.  chart.  No.  vi. 

Sig. — One  every  half-hour  until  reUeved. 

>  Dental  Cosmos,  1910,  p.  1085. 


492         DESTRUCTIVE   DISEASES  OF  THE  DENTAL  PULP 

Trigemin  is  also  useful. 

Quiet  of  the  pulp  must  be  secured  before  an  arsenical  application 
is  made,  or  the  latter  merely  increases  the  irritation  instead  of 
promptly  devitalizing  (an  exception  is  noted  above).  Should  such 
an  irritation  occur  or  be  feared,  arsenic  may  be  sealed  in  an  opening 
made  in  another  part  of  the  tooth  (a  "pocket"  i),  with  a  view  to 
devitalizing  the  pulp  through  an  avenue  of  healthy  pulp  tissue.  At 
the  same  time  the  pulp  may  be  quieted  by  sedative  applications 
made  in  the  cavity  of  decay. 

Instead  of  drilling  a  special  pit,  the  arsenic  may  be  applied  at  a 
portion  of  healthy  dentin  in  the  cavity,  which  is  at  some  distance 
from  the  orifice  of  exposure;  over  the  latter  the  analgesic  may  be 
placed  (see  p.  515,  etc.). 


Fig.  423 


SUPPURATION   OF   THE   PULP. 

Definition. — By  suppuration  of  the  dental  pulp  is  meant  a  forma- 
tion of  pus  on  its  surface  (ulceration)  or  in  its  substance  (abscess). 
It  occurs  both  as  an  acute  and  as  a  chronic  affection. 

Causes. — The  immediate  cause  of  suppuration  of  the  pulp  is  the 
ingress  of  pyogenic  organisms  to  the  pulp.     As  in  inflammation  of 

the  pulp,  while  usually  associated  with 
direct  exposure  of  the  pulp,  suppuration 
may  occur  in  pulps  covered  by  softened 
or  even  unsoftened  dentin. 

Arkovy^  first  observed  infection  of 
the  pulp  while  still  covered  by  a  layer 
of  unsoftened  dentin  (Fig.  423). 

Goadby  has  shown  that  microorgan- 
isms may  penetrate  even  secondary 
dentin,  a  condition  not  infrequently  seen 
(Fig.  423).  Miller  states  that  sections 
of  the  overlying  dentin  in  a  case  of  sup- 
puration of  the  pulp  showed  the  same 
forms  of  bacteria  as  were  found  in  the 
pulp  itself. 
Bacteria  which  have  entered  the  body  through  wounds,  etc.,  may 
be  deposited  in  the  pulp  as  well  as  in  any  other  part  of  the  body, 
wherever  there  may  be  a  lessened  resistance  at  the  time.  While 
bacteria  may  thus  enter  from  the  circulation,  there  is  usually  abun- 
dant opportunity  for  their  entrance  from  the  mouth.     Suppuration 


Invasion  of  pulp  by  micrococci. 
(Arkovy.) 


1  Flagg. 

2  Diagnostik  der  Zahnkrankheiten. 


SUPPURATION  OF  THE  PULP 


493 


of  the  pulp  is  a  not  infrequent  sequel  of  the  capping  of  pulps  which 
have  given  evidence  of  a  previous  hyperemia  or  inflammation. 

Morbid  Anatomy  and  Pathology. — ^Anatomically  pulp  suppuration 
(purulent  or  pyogenic  pulpitis)  is  of  two  general  varieties :  one  begins 
upon  or  close  to  the  suf ace  of  an  exposed  pulp,  and  gradually  destroys 
the  organ  through  a  process  of  progressive  ulceration  (Fig.  424); 
the  second,  that  confined  in  the  substance  of  the  pulp,  causes  the 
gradual  destruction  of  a  part  of  the  pulp  through  the  formation  of 
circumscribed  abscesses  (Fig.  425). 

Fig.  424 


A,  diagram  of  lower  molar  with  caries  at  a  which  exposes  the  pulp;  the  darkened 
portion  at  b  shows  the  extent  of  the  inflammation ;  the  rest  of  the  organ  was  free  from 
inflammatory  change.  B,  illustration  of  the  inflamed  tissue,  showing  a  part  destroyed 
by  suppuration  at  a;  the  odontoblasts  are  undermined  at  b;  the  bloodvessels  which 
were  filled  with  blood  clot  in  the  section  are  left  blank  here,  that  they  may  be  more 
apparent.     (Black.) 


Ulceration  of  the  Pulp. — Of  these  tw^o  forms,  ulceration  is  the 
more  common.  The  capillaries  (Fig.  424)  are  blocked  with  coagu- 
lated blood  (they  are  left  open  in  the  illustration  to  clearly  mark 
their  position);  the  intercapillary  meshwork  is  occupied  by  inflam- 
matory exudation ;  the  surface  of  the  pulp  is  eroded  and  covered  with 
pus  corpuscles;  the  ulcerative  process  is  undermining  the  layer  of 
odontoblasts.  The  suppurative  process  penetrates  the  body  of  the 
pulp,  following  the  direction  of  its  veins  and  hollowing  out  the  organ 


494 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


into  a  deep  cavern.  Black  regards  the  persistence  of  the  layer  of 
odontoblasts  as  indicating  an  inferior  vitality,  as  it  shows  they  are 
less  susceptible  of  change  of  form  than  the  other  cells  of  the  organ. 


Fig.  425 


Acute  suppurative  pulpitis  in  the  coronal  portion;  I,  intensely  inflamed  horn;  A, 
abscess;  V,  bloodvessels  engorged  with  blood;  S,  superficially  inflamed  horn;  N,  nest 
of  inflammation.      X  10.     (Bodecker.) 


The  process  of  ulceration  may  continue  for  weeks  or  months  until 
the  entire  organ  has  been  destroyed  molecularly.  The  necrotic  por- 
tions undergo  putrefactive  decomposition,  probably  passing  through 


SUPPURATION  OF  THE  PULP 


495 


the  same  stages  that  any  albuminous  substance  passes  in  its  serial 
decomposition,  into  the  end-products — ammonia,  carbon  dioxid, 
hydrogen  sulphid,  and  water. 

"Very  interesting  and  instructive  results  were  obtained  by  exam- 
ining the  material  from  different  parts  of  the  same  tooth.  In  the  case 
illustrated  in  Fig.  426  the  pulp  chamber  at  a  was  wide  open  and 
filled  with  food  particles,  which  had  a  foul,  half-putrid  odor;  at  b  the 
pulp  was  putrid  and  foul-smelling;  at  c  there  was  a  small  abscess, 
filled  with  pure  white  pus,  while  the  tissue  between  this  point  and 
the  apex  of  the  root  was  highly  inflamed  and  bright  red.  Material 
from  the  pulp  chamber  (Fig.  426,  a)  contained  the  forms  shown  in 


Fig.  426 


Fig.  427 


Fig.  428 


Fig.  429 


f/ 


Microorganisms  found  in  cultures  from  gangrenous  pulp.     (Miller.) 

Fig.  427;  material  from  point  h  those  shown  in  Fig.  428,  and  from 
the  point  c  those  shown  in  Fig.  429.  We  perceive  a  gradual  dimin- 
ution of  the  large  cocci,  and  the  appearance  of  small,  delicate  cocci 
and  diplococci."  (Miller.^)  The  editor  has  observed  cases  of  vital 
but  finally  ulcerated  pulps  under  canal  fillings.  In  one  case  twelve 
years  had  elapsed  between  the  partial  canal  filling  and  the  more 
recent  observation. 

Symptoms. — If  the  cavity  of  decay  be  open  the  pus  and  serous 
exudate  may  freely  escape,  so  that  the  symptoms  may  not  exceed  a 
dull,  gnawing  pain,  which  is  usually  reflex  in  character. 


I  Dental  Cosmos,  1894. 


496         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

As  a  rule,  the  response  to  cold  will  be  much  delayed  or  even  absent. 
Intense  pain  may  exist  when  the  pus  cannot  find  exit  owing  to  food 
debris  being  massed  in  the  pulp  chamber,  or  owing  to  the  presence 
of  a  filling  or  mass  of  secondary  dentin.  The  case  then  resembles 
and  practically  becomes  one  of  abscess  of  the  pulp. 

The  chief  diagnostic  feature  of  pulp  ulceration  is  the  presence 
of  the  subacute  inflammatory  symptoms  described  above  and  the 
presence  of  a  pulp  partially  removed  by  decomposition  of  its  upper 
portion. 

Thus  if  the  pulp  chamber  be  open  at  one  horn,  and  a  probe  may 
be  passed  into  it  for  a  short  distance  until  it  comes  into  contact  with 
an  irritable  portion  of  pulp,  and  when  withdrawn  have  the  odor  of 
putrefaction,  the  diagnosis  is  clear — loss  of  pulp  substance  by  putre- 
factive changes,  presumably  by  suppuration.  In  some  teeth  it  may 
be  by  partial  gangrene.  Many  phases  of  this  condition  may  be  seen; 
thus  in  an  extreme  case  one  canal  of  a  lower  molar  contained  a  highly 
irritable  vital  filament  of  pulp  extending  but  one-quarter  inch  from 
the  apical  foramen;  a  second  canal  was  entirely  occupied  by  a  per- 
fectly vital  but  ulcerating  filament;  the  third  canal  contained  an 
entirely  dead  pulp.  The  bulb  of  the  pulp  had  disappeared,  doubtless 
by  suppuration. 

Treatment. — ^The  treatment  of  pulp  ulceration  in  its  early  stages 
involves  the  opening  of  the  orifice  of  exposure,  the  sterilization  of 
the  superfices  of  the  pulp,  and  pulp  removal. 

Superficial  sterilization  may  be  accomplished  by  removing  the 
pus  or  putrefactive  material  present  by  means  of  warm  3  per  cent, 
hydrogen  dioxid.  The  saturated  solutions  of  thymol  in  alcohol  or 
menthol  in  chloroform,  or  2  per  cent,  formaldehyd  or  formocresol 
diluted  to  3  per  cent,  formaldehyd  strength  may  be  sealed  in  posi- 
tion against  the  pulp  for  twenty-four  hours  as  an  antiseptic.  The 
application  of  arsenic  may  then  be  safely  made.  In  favorable  cases 
the  bulb  of  the  pulp,  or  even  the  entire  pulp,  may  be  removed  at  the 
first  or  second  sitting  by  means  of  cautiously  applied  cocain  pressure 
anesthesia.  In  some  cases,  however,  the  patient  will  rebel.  (See 
p.  515,  etc.) 

When  a  part  of  the  canal  filaments  alone  remain,  after  syringing 
to  remove  pus,  the  pressure  anesthesia  may  be  resorted  to.  A  long 
thread  of  cotton  is  saturated  with  carbolic  acid  or  carbolic  acid 
and  cocain,  and  gently  packed  into  the  canal  against  the  pulp  fila- 
ment. Pressure  with  vulcanizable  rubber  is  now  produced,  and  after 
a  few  minutes  the  pulp  will  be  sterilized  and  anesthetized  sufficiently 
for  removal.  It  is  better  to  treat  each  canal  separately  as  a  general 
pressure  will  probably  fail.     Puncturing  is  also  useful  at  times  (see  p. 


SUPPURATION  OF  THE  PULP  497 

531).  Arsenic  may  be  cautiously  placed  on  cotton  half-way  up  a 
canal  against  such  a  pulp  filament.  Another  method  consists  of 
packing  a  thread  of  cotton  dipped  in  carbolic  acid  tightly  against 
the  filament,  in  which  thrombosis  is  thus  induced.  (See  also  p. 
531.) 

Abscess  of  the  Pulp. — Abscess  of  the  pulp  is  usually  situated  near 
the  point  of  exposure  of  the  organ.  It  may  be  confined  to  one  horn 
of  the  pulp,  or  may  involve  nearly  the  entire  substance  of  the  pulp, 
the  peripheral  tissue  of  the  pulp  being  unbroken.  Abscess  may  exist 
at  some  distance  beneath  the  surface  of  the  pulp,  and  the  latter  be 
still  covered  with  a  layer  of  dentin.  Burchard  once  uncovered  the 
horn  of  a  molar  pulp  which  was  covered  by  a  lamina  of  hard  dentin, 
and  no  fluid  appeared;  but  upon  passing  a  sharp  probe  into  the  white 
area  of  exposure  for  over  one-eighth  of  an  inch  or  more  there  was  a 
free  flow  of  pus  which  quickly  filled  the  larger  carious  cavity.  A  pulp 
removed  entire  from  a  tooth,  and  which  was  yellowish  white  in  color 
and  unbroken,  showed  upon  section  its  interior  hollowed  out  into  an 
enormous  abscess  cavity  (Fig.  431).  The  bloodvessels  were  blocked; 
the  peripheral  tissues  were  unaltered;  between  the  odontoblasts  and 
the  abscess  cavity,  the  latter  lined  with  pus  corpuscles,  evidences  of 
inflammation  were  plenty.  Black  found  that  the  odontoblasts 
retained  their  form  after  neighboring  cells  of  the  pulp  had  been 
destroyed. 

Miller's^  researches  show  a  preponderance  of  cocci  and  micrococci 
in  cases  of  enclosed  abscess;  cocci  and  diplococci  were  of  constant 
occurrence.  Many  of  the  forms,  both  cocci  and  bacilli,  were  cultivable 
upon  gelatin  and  agar-agar.  Some  of  them,  cocci  and  bacilli,  brought 
about  the  liquefaction  of  gelatin;  other  did  not.  So  that  it  must  be 
inferred  that  infective  inflammation  and  necrosis  of  the  pulp  may 
occur  without  suppuration.  (See  Gangrene  of  the  Pulp.)  In  some 
instances  streptococci  were  found.  In  the  freely  exposed  pulps 
varieties  of  organisms  were  found  which  would  render  clear  the 
possibility  of  a  general  infection  by  way  of  the  dental  pulp. 

Symptoms. — The  usual  symptoms  are  as  follows:  In  a  tooth  con- 
taining an  enormous  filling,  one  in  which  the  pulp  has  been  exposed, 
or  in  a  tooth  having  a  large  carious  cavity,  the  patient  gives  a  history 
of  discomfort  or  decided  pain,  appearing  at  intervals,  sometimes 
appearing  and  disappearing  suddenly,  the  existing  condition  having 
been  ushered  in  by  dull,  gnawing  pain,  which  is  usually  not  positively 
located,  although  it  may  be.  The  pain  grows  in  intensity,  and,  in 
contradistinction  to  the  pulp  conditions  previously  described,  pain 

1  Dental  Cosmos,  1894. 
32 


498 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


is  relieved  instead  of  increased  by  applications  of  cold.     It  may  be, 
however,  that  the  prolonged  contact  of  iced  water  may  induce  a 


Fig.  431 


Fig.  432 


Transverse  section  of  inferior  bicuspid  pulp,  one-half  diagrammatic:  a,  abscess 
cavity;  b,  embryonic  cells  at  the  periphery  of  the  abscess  cavity;  c,  occluded  blood- 
vessels.    (Burchard.) 

response.    The  response  to  heat  is  marked,  so  that  a  mouthful  of  hot 
coffee  or  even  the  warmth  of  the  tongue  may  precipitate  an  attack 

of  severe  and  continued  pain. 
Pain  produced  upon  passing  from 
a  warm  to  a  cold  atmosphere,  and 
vice  versa,  is  also  symptomatic.  If 
the  pulp  be  freely  exposed  and 
pricked  with  a  sharp  instrument,  a 
flow  of  pus  follows  in  many  cases, 
and  the  relief  is  almost  immediate. 
In  the  earlier  stages  a  period  of 
throbbing  pain  may  follow  evacu- 
ation of  the  pus. 

In  other  cases  the  response  to 
heat  may  decrease  until  it  is  almost 
absent,  and  the  case  only  be  seen 
when  evidences  of  the  action  of 
bacterial  products  upon  the  peri- 
cementum appear,  which  they 
usually  do  in  the  later  stages  of  pulp  suppuration,  when  the  tooth 
becomes  loose,  extruded,  and  tender  upon  percussion. 


Abscess  of  the  pulp  after  forma- 
tion of  a  large  amount  of  secondary 
dentin,  dividing  the  pulp  into  two 
portions:  ;S  D,  secondary  dentin; 
V  P,  abscess  or  confined  pus;  I, 
area  of  apical  inflammation.  (Dia- 
grammatic.) (After  case  in  the 
mouth.) 


SUPPURATION  OF  THE  PULP  499 

The  symptoms  of  pericemental  disturbance  may  simulate  those  of 
incipient,  acute,  apical  abscess,  even  though  a  quarter  of  an  inch  or 
more  of  apical  pulp  tissue  exist  in  a  vital  though  highly  inflamed 
condition.  Upon  clinical  evidence  it  is  assumed  that  the  inflammation 
of  the  pulp  produces  inflammation  of  the  apical  tissue  (Fig.  432). 
In  one  case  the  gum  and  contiguous  parts  about  an  upper  molar 
were  swollen,  apical  abscess  diagnosticated,  and  a  free  flow  of  pus 
followed  by  blood  obtained  upon  opening  the  crown.  An  examina- 
tion made  twenty-four  hours  later,  after  symptoms  had  subsided, 
demonstrated  all  three  pulp  filaments  to  be  alive  when  a  post  hoc 
diagnosis  of  extensive  abscess  of  the  pulp  was  made.  If  untreated, 
symptoms  of  pulp  and  pericemental  disturbance  may  disappear  for 
weeks  or  months;  but  if  the  parts  be  not  perfectly  sterilized  and 
reinfection  prevented,  it  is  only  a  question  of  time  when  septic 
pericementitis  will  arise. 

Diagnosis. — The  most  valuable  diagnostic  symptom  is  the  peculiar 
reaction  to  thermal  stimuli — the  decreasing,  then  absent  response 
to  cold,  and  the  increasing  reaction  to  applications  of  heat.  This 
reaction,  together  with  the  continued  gnawing  and  full  sensation 
in  the  tooth,  usually  affords  a  diagnosis  which  is  confirmed  by  evac- 
uating pus  from  the  pulp,  which  exudes  usually  as  a  minute  bead 
followed  by  blood,  although  the  reverse  order  may  obtain. 

In  cases  where  several  teeth  are  involved  in  the  diagnosis,  differ- 
entiation is  made  by  isolation  of  each  tooth  by  means  of  a  small 
square  of  rubber  dam.  The  thermal  test  is  then  applied.  The  pres- 
ence of  a  quantity  of  secondary  dentin  will  confuse  by  causing  dulness 
of  response.  In  such  case  the  electric  test  should  be  resorted  to. 
(See  Dry  Gangrene.)  In  some  cases  secondary  dentin  will  have 
formed  in  the  pulp  cavity  and  the  abscess  may  be  found  in  one  of 
the  filaments,  while  the  other  will  be  apparently  healthy.  Fig.  432 
is  a  diagram  of  a  number  of  cases  seen  in  practice. 

Prognosis. — General  experience  regards  ulceration  and  abscess  of 
the  pulp  as  precursors  of  the  death  of  the  organ.  Usually  this  is 
by  progressive  suppuration.  It  is  undoubtedly  true,  however,  that 
attempts  at  circumvallation  of  the  dead  tissue  are  made  in  some 
cases  (Fig.  433).  The  pus  cells  undergo  degeneration  and  the  abscess 
site  may  be  the  seat  of  calcareous  deposits.  Even  in  these  cases 
death  is  delayed,  not  averted.  The  remainder  of  the  pulp  under- 
goes atrophic  changes,  and  commonly  suppuration  reappears. 

Treatment.- — The  treatment  of  the  case  consists  in  relieving  the 
existing  pain,  completing  the  devitalization  of  the  pulp,  and  removing 
it  in  such  a  manner  that  no  organisms  or  dead  matter  are  carried 
beyond  the  apex  of  the  root. 


500 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


To  secure  relief,  evacuation  of  the  pus  is  imperatively  necessary. 
The  organ  is  freely  exposed,  exercising  no  pressure  in  gaining  free 
access  to  it.     If  pus  does  not  flow  upon  exposure  of  the  surface  of 


Fig.  433 


Chronic  suppurative  pulpitis  terminating  in  calcification  of  the  pus  and  atrophy  of 
the  pulp:  A^,  larger  abscess,  filled  with  calcified  pus;  A^,  abscess  at  the  periphery  of 
the  pulp;  A^,  A^,  small  longitudinal  abscesses,  all  calcified;  N,  calcified  nerve  bundle; 
C,  C,  calcareous  depositions  in  the  fibrous  pulp  tissue;  P,  P,  pigment  clusters  from 
previous  hemorrhage.      X  10.     (Bodecker.) 


the  pulp,  a  sharp,  slender,  sterilized  probe  is  quickly  passed  into  the 
substance  of  the  pulp,  when,  if  pus  be  present,  it  will  usually  escape 
freely  through  the  opening  thus  made  and  be  followed  by  blood. 


CHRONIC  INFLAMMATION  OF  THE  PULP 


501 


If  the  pus  formation  be  limited  and  circumscribed,  throbbing 
pain  may  follow,  which  a  sedative  promptly  quiets.  The  application 
is  not  made  until  the  pus  flow  ceases.  A  pellet  of  cotton  wet  with  a 
1  per  cent,  solution  of  formalin,  or  a  saturated  solution  of  thymol 
in  alcohol  or  other  antiseptic  sedative,  is  laid  upon  the  pulp  and 
the  cavity  is  sealed  for  twenty-four  hours  (never  longer),  and  then 
the  pulp  is  removed.  Should  the  exposed  portion  of  the  pulp  be 
insensitive  it  is  cut  away  until  access  is  had  to  the  vital  portion, 
where  the  arsenic  is  to  be  applied.  The  pulp  may  sometimes  be 
anesthetized  by  cocain  for  removal.  The  rubber  dam  need  not 
necessarily  be  applied  for  the  treatment  preliminary  to  devitalization, 
but  the  pulp  should  be  kept  under  the  influence  of  antiseptics.  (See 
p.  515,  etc.) 

CHRONIC   INFLAMMATION   OF   THE   PULP. 

In  cases  in  which  the  resistive  force  of  the  pulp  is  great  and  the 
causes  of  less  violent  nature  or  less  violent  in  action,  the  inflammation 
may  be  of  low  grade  and  continue  for  some  time.  Pulp  ulceration 
may  pursue  a  chronic  course,  as  has  already  been  described.  Abscess 
of  the  pulp  may  also  become  chronic,  and  the  pulp  may  even  encap- 
sule  the  pus  area,  and,  the  bacteria  dying,  the  abscess  area  may 
become  the  seat  of  calcareous  deposits. 

Fig.  434 


Chronic  inflammation  of  the  pulp,  areolation,  and  degeneration      (Black.) 

Sclerosis  of  the  Pulp. — Inflammation  of  a  low  grade  may  persist 
in  the  pulp  for  long  periods,  giving  rise  to  an  increase  of  its  fibrous 
tissue  with  atrophy  of  the  cellular  elements,  producing  a  condition 
found  in  chronic  interstitial  inflammation  in  some  other  tissues — a 
sclerosis.  Instead  of  the  usual  distribution  of  mjTiomatous  tissue, 
bands  and  bundles  of  fibrous  tissue  appear.  The  pulp  appears 
shrunken  and  stiff,  bloodvessels  are  contracted  and  sclerotic,  and 
the  nerve  fibres  have  undergone  partial  or  complete  atrophy  and 
degeneration  (Figs.  434  and  4.35). 


Fig.  435 


Pulpitis  arteriosclerosis;  nerve  degeneration.     (V.  A.  Latham.) 
Fig.  436 


A,  a  first  lower  molar  with  a  cavity  at  a  completely  fiUed  by  an  hypertrophy  of  the 
pulp,  which  has  grown  out  through  the  orifice,  exposing  the  pulp  at  b.  B,  a  field 
illustrating  the  tissue  of  the  growth,  which  is  composed  almost  entirely  of  granulation 
tissue  of  a  very  primitive  type;  a,  a  covering  of  epithelium  presenting  papillae ;  b, 
epithelium  apparently  without  papillae.    (Black.) 


CHRONIC  INFLAMMATION  OF  THE  PULP  503 

Black  found  that  in  the  late  stages  of  sclerotic  atrophy  areolae 
developed  in  the  bundles  of  connective  tissue,  the  inflammatory 
elements  having  disappeared  and  the  areolse  being  occupied  by 
fluid.  Arkovy  describes  the  condition  as  reticular  atrophy  of  the 
pulp  (Fig.  434). 

Sclerotic  and  other  chronic  degenerations  of  the  pulp  usually 
present  the  history  of  one  or  more  attacks  of  pulpitis  in  the  past, 
with  more  or  less  continuous  uneasiness  extending  over  a  long  period. 
The  response  of  the  pulp  to  all  tests  becomes  diminished  and  dull. 
Treatment.— Such  pulps  are  to  be  devitalized  and  removed. 
Chronic  Hyperplastic  (Hypertrophic)  Pulpitis.— When  the  pulp 
is  exposed  over  a  wide  area,  long-continued  chronic  inflammation 
may  lead  to  an  enlargement  of  the  organ  with  a  protrusion  of  an 
altered  pulp  mass  through  the  orifice  of  exposure,  producing  the 
condition  known  clinically  as  fungous  pulp.  When  the  growth 
extends  beyond  the  boundaries  of  the  orifice  and  then  increases  in 
bulk  it  forms  a  pedunculated  mass  to  which  the  term  polypus  of  the 
pulp  has  been  applied. 

Morbid  Anatomy  and  Pathology.— The  growth  has  its  origin  in  a 
chronic  inflammation  of  the  body  of  the  pulp;  the  organ  swells,  and 
contact  with  the  sharp  edges  of  the  orifice  of  exposure  excites  a 
continued  irritation,  leading  to  further  proliferation  of  the  cells  of 
the  inflamed  part,  so  that  a  large  mass  of  embryonic  tissue  is  formed 
(Fig.  436),  termed  by  Black  granulation  tissue  of  a  low  type.  As  in 
the  granulation  tissue  of  repair,  bloodvessels  grow  into  this  mass, 
so  that  it  may  bleed  at  a  slight  touch.  Black  noted  in  his  case  illus- 
trated, a  covering  of  squamous  epithelium  upon  the  periphery  of  the 
growth,  which  might  be  interpreted  as  the  transformation  of  meso- 
blastic  into  epiblastic  tissue,  but  the  correct  explanation  beyond 
doubt  is  that  advanced  by  the  same  author,  that  the  epithelium  is 
transplanted  from  the  gums,  and  grows  after  the  manner  of  a  skin 
graft.  The  growth  does  not  contain  nerves.  The  cavity  in  which  it 
lies  is  often  fairly  free  from  decalcified  dentin,  the  walls  appearing  as 
though  subjected  to  an  absorbent  action. 

These  growths  may  undergo  further  changes;  higher  organization 
of  the  granulation  tissue  occurs  and  fibrous  tissue  is  formed;  the  cells 
may  undergo  degenerations,  first  granular,  then  fatty,  and  suppura- 
tion and  gangrene  may  occur.  Tomes^  records  a  case  where  calci- 
fication of  an  hypertrophied  section  of  a  pulp  occurred;  but  as  the 
case  was  due  to  traumatism  (fracture  of  a  tooth),  different  vital 
conditions  existed  from  those  in  the  cases  under  discussion.    Actual 

1  Dental  Surgery,  third  edition. 


504 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


calcification  of  the  mass  is  scarcely  possible,  although  calcareous 
degeneration  may  occur  within  the  fungous  mass  (Fig.  437,  G). 

While  the  growth  occupies  a  cavity  of  decay,  it  seems  at  times  to 
have  acted  upon  the  carious  dentin  so  as  to  remove  it  by  absorption, 
leaving  the  cavity  more  or  less  clean. 

Fig.  437 


Hyperplastic  myxomatous  pulp,  which  filled  a  carious  cavity:  M,  lobules  made  up 
of  papillae  of  a  myxomatous  structure,  rich  in  capillary  and  venous  bloodvessels;  G, 
calcareous  globule;  S,  epithelial  cover  of  papillae.     X  10.     (Bodecker.) 


Resorption  of  the  walls  of  the  pulp  chamber  may  occur  as  an 
accompaniment  of  chronic  pulpitis.  What  appears  to  be  an  idio- 
pathic dentin  resorption  is  described  on  p.  487.  Black  records  a 
case  where,  after  pulp  capping  in  a  lower  molar  and  the  insertion 
of  a  large  gold  filling,  the  tooth  was  examined  at  the  end  of  ten  years; 
for  two  or  three  years  the  pulp  had  given  evidences  of  irritability, 
and  when  the  pulp  was  removed  the  pulp  chamber  was  found  enor- 


CHRONIC  INFLAMMATION  OF  THE  PULP 


505 


mously  enlarged  and  opening  into  the  pericementum  between  the 
roots  of  the  teeth.  Fig.  438  exhibits  resorption  of  previously  formed 
secondary   dentin   with    the   probable   agency   through   which   the 


Fig.  438 


Acute  pulpitis:  S,  secondary  dentin;  B,  bay-like  excavations  filled  with  medullary 
or  inflammatory  corpuscles;  V,  transverse  section  of  a  bloodvessel;  M,  multinuclear 
body,     X  300.     (Bodecker.) 

resorption  is  brought  about.  The  area  of  resorption  is  invaded  by 
numerous  multinucleated  cells,  which  are  evidently  performing  the 
function  of  odontoblasts. 


Fig.  439 


Fig.  440 


Fig.  441 


Fig.  442 


Hypertrophy  of  pulps.  (Garreston.) 


As  shown  by  Miller,  Hopewell-Smith,  and  others,  a  reconstructive 
change  may  occur  and  adventitious  dentin  be  redeposited  in  the 
area  of  resorption  (Fig.  422). 

Symptoms. — ^The  symptoms  of  chronic  pulp  inflammations  and 
degenerations  are  usually  those  of  long-continued  discomfort,  with 


506         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

reflex  pains,  which  rarely  persist  into  the  latest  stages  of  degeneration. 
The  response  to  heat  and  cold,  present  at  first,  declines  until  the 
pulp  scarcely  reacts,  and  then  but  slowly. 

No  nerve  fibres  develop  in  the  hypertrophic  pulp  tissue,  so  that 
the  newgrowth  has  no  sensitivity  in  itself,  although  pressure  upon  it 
may  cause  sharp  pain  through  the  still  vital  pulp  nerves  themselves. 

Four  or  five  of  these  hypertrophies  may  exist  in  a  mouth,  filling 
whole  cavities  of  decay,  the  surrounding  tooth  structure  being  in 
various  stages  of  disintegration.  They  seem  to  be  comparatively 
insensitive  to  mastication  (Fig.  440). 

Fig.  443  Fig.  444 


Hypertrophy  of  the  gum.  Hypertrophy  of  the  pericementum. 

(Garretson.)  (Garretson.) 

Hypertrophy  of  the  pulp  also  may  be  associated  with  pulp  ulcera- 
tion, the  growth  arising  from  one  canal  of  a  tooth. 

Regeneration  of  an  extirpated  pulp  has  been  claimed.  These  are 
probably  referable  to  the  above  form  of  hypertrophy,  or  to  a  fungoid 
growth  from  the  pericementum  or  supposed  extirpation  under  cocaine. 

Diagnosis. — The  only  condition  with  which  hypertrophic  pulp  may 
be  confounded  is  a  pedunculated  growth  of  gum  tissue  through  a 
cavity  at  the  neck  of  a  tooth  beneath  the  gum  margin,  or  through 
a  perforation  either  accidental  or  by  caries  (Fig.  444).  It  is  impor- 
tant to  difl'erentiate  between  these  conditions,  because,  if  an  appli- 
cation of  arsenical  paste  be  made  to  a  fungous  gum,  the  destruction 
of  tissue  may  extend  into  the  sound  pericementum.  The  physical 
appearances  of  the  two  are  alike;  they  both  bleed  freely  and  have 
about  the  same  degree  of  sensitivity. 

Histological  examination  of  this  class  of  hypertrophy  of  the  gums, 
conducted  by  Dr.  Luigi  Ancone,^  of  Italy,  demonstrated  that  the 
growth  is  a  simple  exaggeration  of  the  normal  elements  of  the  part. 

If  the  tumor  be  central  to  the  tooth  tissue  and  the  latter  not 
decayed  out  to  very  thin  walls,  it  may  be  at  times  laid  aside  by  means 
of  a  blunt  instrument  and  be  seen  to  have  its  origin  from  an  orifice  of 
exposure  (Fig.  439).     As  a  rule,  a  hyperplastic  pericementum  will 

1  Abstract  from  I'Odontologia,  by  Dr.  W.  Dunn,  in  International  Dental  Journal,  1899. 


CHRONIC  INFLAMMATION  OF  THE  PULP  507 

be  found  to  have  its  attachment  much  lower  or  more  lateral  than 
a  hyperplastic  pulp,  and  the  pulp  cavity  be  seen  to  have  been  enlarged 
by  caries,  even  more  than  shown  in  Fig.  362.  It  is  then  fairly  inferred 
to  be  a  gum  mass,  especially  if  the  tooth  has  never  been  operated 
upon.  The  diagnosis  may  be  a  doubtful  one,  in  which  case  the 
rubber  dam  is  to  be  applied,  the  polypus  frozen  by  means  of  a  spray 
of  ethyl  or  methyl  chlorid,  and  the  mass  removed  with  a  sharp 
blade  passed  across  its  peduncle.  The  electric  cautery  may  be  used 
to  ablate  the  mass. 

The  source  of  the  tumor  may  then  be  usually  clearly  seen.  As  an 
alternative  proceeding  the  tissue  may  be  thoroughly  saturated  with  a 
strong  solution  of  trichloracetic  acid  and  then  ablated.  If  any  fur- 
ther doubt  exist,  the  pulp  is  to  be  sterilized  with  hydrogen  dioxid,  etc., 
and  a  pellet  of  cotton  saturated  with  oil  of  cloves,  carbolic  acid,  or 
dental  tincture  of  iodin  is  laid  upon  it,  and  over  this  temporary  stop- 
ping is  firmly  packed.  By  this  means  the  growth  may  be  pressed 
away  until  it  is  seen  to  arise  from  either  a  pulp  chamber  or  a  perfora- 
tion made  by  decay  or  accidental  excavation  into  the  pericemental 
tract. 

Pressure  anesthesia  may  be  resorted  to  partly  as  a  diagnostic 
measure.  In  such  case  no  danger  exists  beyond  the  possible  forcing 
of  cocain  into  the  gum  tissue.  Nervocidin  should  be  useful  in  cases 
of  doubt.  Skiagraphy  should  afford  a  diagnosis.  Hemorrhage  may 
be  checked  with  alum  and  thymol  in  powder  or  solution,  or  by  the 
use  of  trichloracetic  acid,  silver  nitrate,  zinc  chlorid,  or  iodin. 

Treatment. — If  the  case  be  one  of  pulp  hypertrophy,  arsenic  may 
be  applied  or  pressure  anesthesia  attempted  for  pulp  removal. 

Crystals  of  iodin  have  heen  used  with  satisfaction  in  combination 
with  pressure  for  pulp  devitalization .  ^  If  a  perforation  exist,  it  is  to 
be  treated  by  sealing  the  orifice  with  gutta-percha,  copper  amalgam, 
or  oxyphosphate  of  copper  cement.    (See  p.  561.) 

Infarction  of  the  Pulp. — The  production  of  infarction  may  result 
as  described  under  Fibroid  Degeneration,  and  as  described  consists 
of  minute  circumscribed  hemorrhages  from  end  arteries  into  the  pulp 
tissue.  This  differs  somewhat  from  a  true  infarction.  (See  p.  119, 
and  Fig.  445.) 

Fibroid  Degeneration  of  the  Pulp. — Apart  from  the  degenerations 
due  to  inflammatory  conditions,  a  form  of  degeneration  occurs  "as  a 
natural  old-age  termination  of  the  life  of  a  healthy  pulp,  and  similar 
to  senile  changes  occurring  in  the  pericementum."  (See  Fibroid 
Degeneration   of   Pericementum).     This   change,   as  described  by 

1  Truman. 


508 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


Hopewell-Smith/  occurs  in  teeth  of  the  aged  in  whose  mouths  simple 
alveolar  resorption  has  occurred,  though  later  he^  has  shown  that  it 
may  occur  in  the  pulps  of  young  persons,  in  sound  teeth  extracted 
for  irregularity,  and  even  in  teeth  in  which  the  dentinal  wall  or  pulp 
cavity  is  not  completed  to  a  typical  calcification.     He  regards  it 

Fig.  445 


H,  hemorrhagic  infarct;  R,  rupture  of  bloodvessel;  D,  dentin;  O,  vacuolated  odonto- 
blasts; F,  early  fibrosis  of  pulp.    X  250.   (Hopewell-Smith.) 

as  due  to  a  primary  thrombosis  of  the  capillaries  and  veins,  with 
permanent  dilatation  of  the  arteries,  with  or  without  tiny  hemor- 
rhages, the  lack  of  collateral  circulation  and  lymphatics  con- 
tributing to  the  atrophy.  As  a  cause  he  suggests  chemical  change 
in  the  blood  through  systemic  derangement,  as  anemia,  chlorosis, 
or  exhaustive    diseases,   the  red  corpuscles    being  fewer  and   the 


1  Histology  and  Pathohistology  of  the  Teeth. 


2  Dental  Cosmos,  1907. 


CHRONIC  INFLAMMATION  OF  THE  PULP 


509 


leukocytes  and  blood  platelets  increased,  thus  favoring  a  thrombosis 
of  small  vessels;  also,  that  here  inflammatory  changes  in  the  peri- 


DO 


Fig.  446 


Horizontal  section  of  fibroid  degeneration  of  the  pulp  in  situ.  Prepared  by  Mr. 
Hopewell-Smith's  process:  D,  deeply  stained  dentin;  <S,  large  areollar  spaces;  DO, 
degenerate  odontoblasts;  P,  fibroid  tissue  of  pulp.      X  45.     (Hopewel-Smith.) 


cemental  tissue  might  interfere  with  the  pulp  circulation  sufhciently 
to  produce  it. 


510 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 


Clinical  Significance. — ^While  the  form  of  thrombosis  or  fibrosis 
may  not  be  diagnosticated  because  of  lack  of  related  symptoms, 
Hopewell-Smith  argues  that  they  should  be  suspected  in  weak  and 
unhealthy  patients,  and  that  such  suspicion  should  contra-indicate 
conservative  operations,  also  that  they  may  explain  certain  difficulties 
of  devitalization  or  anesthetization  of  the  pulp  or  cause  a  related 
change  in  the  pericementum  or  brittleness  in  the  dentin. 

Fig.  447 


■FO 


Fibroid  degeneration  of  the  pulp:  D,  dentin  with  tubules;  FO,  fibroid  odontoblasts; 
P,  atrophied  pulp  tissue. 


Morbid  Anatomy. — "The  odontoblasts  become  sheaved  with  or 
without  fatty  degeneration;  the  arteries,  permanently  distended, 
undergo  hyaline  degeneration;  a  reticular  atrophy  occurs,  with  dis- 
appearance of  cells  and  nuclei  of  both  pulp  and  vessels  and  nerves, 
and,  at  the  same  time,  the  connective-tissue  fibres  undergo  hyper- 
plasia. The  pulp  goes  more  or  less  gradually  through  the  stages 
shown  in  Fig.  445,  finally  producing  the  stage  shown  in  Figs.  446 
and  447,  in  which  the  pulps  are  shrunken  and  may  have  left  the  wall 
of  the  pulp  chamber.  "Many  areolar  spaces  appear  which  may  be 
arranged  in  chains.    The  odontoblasts  are  degenerated.    The  pulp 


CHRONIC  INFLAMMATION  OF  THE  PULP 


511 


stroma  is  very  dense,  has  a  clear,  fibrous  structure,  becomes  very 
marked  in  staining,  and  is  highly  differentiated  from  the  surrounding 
tissue.  The  bloodvessels,  nerves,  cells,  and  connective-tissue  have 
all  disappeared,  and  their  place  is  taken  by  a  new,  firm,  fibrous 
structure  devoid  of  cells,  nuclei,  or  any  regular  arrangement  of 
constituent  parts." 

Fig.  448 


Fatty  degeneration  of  the  pulp.   (V.  A.  Latham.) 


"There  is  no  calcification  of  the  pulp  and  no  obliteration  of  the 
dentinal  tubules. 

"The  proximate  cause  and  associate  phenomena  are  not  as  yet 
clearly  related." 

Fatty  Degeneration  of  the  Pulp. — During  the  course  of  degenera- 
tion of  the  elements  of  the  pulp  fatty  changes  may  occur  as  in  other 
parts.  The  fatty  changes  occur  in  the  walls  of  the  arteries  and 
sheaths  of  the  nerves,  and  in  the  odontoblasts.    (Hopewell-Smith.) 

Cloudy  swelling  also  appears.     (Latham.)     (See  Fig.  512.) 


512 


DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 
Fig.  449 


.^,.„57^>^- :  ,:jF?isr--7' 


^-/^^:^:.  -Jff.!,/;2>vl 


Cloudy  swelling;  parenchymatous  degeneration;  pulp  nodules.   (V.  A.  Latham. 0 

Fig.  450 


Colloid  degeneration  of  the  pulp.     Compare  with  Fig.  49.      (V.  A.  Latham.) 

1  Dr.  Vida  A.  Latham's  illustrations  are  from  her  paper  on  Some  Pathological 
Features  of  the  Pulp,  Journal  of  the  American  Medical  Association,  September  22, 
1906. 


CHRONIC  INFLAMMATION  OF  THE  PULP  513 

Fig.  451 


Great  thickening^of  nerve  bundle.     From  a  case  of  chronic  neuralgia.     Patient  had 
many  teeth  extracted  for  neuritis.   (V.  A.  Latham.) 


Fig.  452 


33 


Neoplasm  of  the  pulp.     (V.  A.  Latham.) 


514         DESTRUCTIVE  DISEASES  OF  THE  DENTAL  PULP 

Colloid  Degeneration  of  the  Pulp. — The  demonstration  of  colloid 
material  within  the  pulp  has  been  made  by  Latham,  as  shown  in 
Fig.  450.  She  states  that  it  may  become  calcified.  The  condition 
is  very  rare.  Other  degenerations  such  as  Wallerian,  hyaline,  and 
amyloid  have  been  noted. ^  It  would  seem  that  the  pulp  may  be 
subject  to  any  form  of  degeneration  seen  elsewhere. 

Nerve-end  Degeneration  of  the  Pulp. — The  degeneration  of  nerves 
occurs  in  the  pulp  as  it  may  in  the  pericementum  and  from  the 
same  causes  that  produce  endarteritis.  The  bundles  may  be  enlarged. 
Neuralgia  may  be  associated  with  it. 

Neoplasm  of  the  Pulp. — Latham  claims  that  a  neoplasm  may  occur 
in  the  pulp,  and  ofi^ers  the  photomicrograph  shown  in  Fig.  452  as 
proof  of  the  fact.  I  do  not  know  of  any  cases  in  which  such  a  pulp 
condition  has  been  related  with  a  malignant  growth  outside  of  the 
pulp  cavity,  though  it  may  not  be  impossible. 

Many  of  the  destructive  pulp  diseases  occur  in  the  pulps  of  the 
temporary  teeth,  and  are  to  be  treated  in  like  manner,  except  as  to 
the  use  of  arsenic,  which,  being  accompanied  by  greater  danger, 
should,  for  the  most  part,  be  replaced  by  other  methods  of  pulp 
removal.  This  point  is  discussed  at  length  in  the  chapter  upon 
Removal  of  the  Pulp. 

If  the  tooth  roots  be  largely  resorbed,  the  pulp  may  bear  capping 
even  when  ulceration  has  occurred.  The  pulp  may  die  under  this 
capping,  when  the  case  is  further  treated  as  indicated.  (See  Chronic 
Apical  Abscess.) 

1  Talbot:  Dental  Cosmos,  1909,  p.  1150. 


CHAPTER  XVII. 

METHODS  OF  REMOVAL  OF  THE  DENTAL  PULP 
AND  ROOT-CANAL  FILLING. 

There  are  four  general  methods  by  which  a  patient  or  pulp  may 
be  prepared  for  the  operation  of  pulp  extirpation.  These  are  as 
follows : 

L  Anesthetization  of  the  patient  and  removal  of  the  pulp  during 
the  period  of  anesthesia. 

2.  Anesthetization  of  the  pulp  by  cocain  or  novocain,  or  in  some 
cases  by  nervocidin,  and  the  removal  of  the  pulp. 

3.  Anesthetization  of  the  apical  tissue  with  novocain  by  the  mucous 
or  conductive  method  and  removal  of  the  pulp. 

4.  Devitalization  of  the  pulp  followed  by  its  removal. 

L  General  Anesthesia. — The  pulp  of  a  single-rooted  tooth  may  be 
readily  extirpated  while  the  patient  is  anesthetized  by  nitrous  oxid, 
nitrous  oxid  and  oxygen,  or  by  somnoform.  The  instruments  should 
be  in  readiness,  the  patient  anesthetized,  the  pulp  uncovered  by 
an  engine  bur,  and  the  pulp  extirpated  with  a  barbed  broach  or 
Donaldson  cleanser. 

In  cases  of  multirooted  teeth  the  available  anesthetics  are  ether, 
which  is  rarely  used  for  the  purpose,  and  nitrous  oxid  and  oxygen 
administered  by  nasal  inhalation.  The  latter  is  accomplished  by 
means  of  a  special  apparatus  having  a  hood  covering  the  nose,  or 
bulbs  entering  the  nostrils.  This  is  designed  to  prolong  the  anesthesia 
by  administering  nitrous  oxid  and  oxygen.  As  it  is  equally  appli- 
cable to  the  excavation  of  cavities  of  decay  and  extractions,  it  is 
a  valuable  means  for  this  purpose.     (See  p.  398.) 

The  ordinary  outfit  is,  however,  of  value  by  enabling  the  operator 
to  remove  the  diseased  bulb  of  the  pulp  of  a  multirooted  tooth,  after 
which  and  while  the  patient  is  conscious  other  methods  of  removal 
of  the  radicular  portions  of  the  pulp  may  be  employed.    (See  p.  49L) 

2.  Anesthesia  of  the  Pulp. — For  this  purpose  cocain  hydrochlorid 
or  novocain  are  employed.  There  are  three  practical  methods  by 
which  it  may  be  introduced  into  a  pulp : 

(a)  By  pressure  accomplished  by  means  of  raw  vulcanite.  A  strong 
solution  (50  per  cent,  to  saturated  solution)  of  cocain  hydrochlorid 
or  novocain  is  made  in  water,  or  preferably  in  some  mild  antiseptic 

(515) 


516      REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

solution  which  does  not  cloud  on  admixture  (as  Borine)  A  small 
piece  of  amadou  (spunk)  is  saturated  with  it  and  laid  upon  the  orifice 
of  exposure.  The  cavity  is  filled  with  the  rubber,  and  upon  this  is 
placed  a  flat-ended  plugger  or  burnisher  broad  enough  to  concentrate 
the  force  upon  the  amadou.  A  broad  piece  of  amadou  placed  over 
the  rubber  is  sometimes  of  assistance  in  preventing  the  slipping 
about  of  the  rubber.  Gentle  pressure  is  now  made  and  a  slight  pain 
is  usually  felt.  The  pressure  should  be  maintained  until  this  passes 
away,  then  it  is  increased  little  by  little  until  some  force  is  exerted. 
The  rubber  and  amadou  are  then  removed,  the  pulp  cavity  opened, 
the  progress  of  the  anesthesia  tested  with  a  fine  broach,  and  the  pulp 
lifted  away.  Some  prefer  to  place  a  prepared  pellet  of  cocain  or 
novocain  upon  the  pulp. 

For  multirooted  teeth  the  pressure  should  be  prolonged,  and  to 
prevent  return  of  sensation  and  hemorrhage  while  extirpating  it  is 
well  to  instil  carbolic  acid  into  the  pulp  tissue  by  means  of  a  fine, 
smooth  broach. 

In  some  cases  the  operation  fails  because  the  direction  of  the 
pressure  has  been  away  from  the  pulp  or  because  the  spunk  has 
slipped  from  its  place.  Sometimes  the  orifice  of  exposure  may  be 
enlarged,  but  as  sensation  is  discovered  a  fresh  application  must  be 
made.  In  cases  with  large  foramina  the  application  may  fail;  with 
the  incomplete  foramen  of  moderate  size  it  is  more  successful. 

Sometimes  repeated  applications  fail  to  effect,  though  the  appli- 
cation is  not  painful,  and  at  times  the  pressure  is  not  tolerated  at 
all,  owing  to  the  irritability  of  the  pulp,  due  to  continued  hyperemia 
or  inflammation.  Even  six  or  eight  applications  have  at  times 
failed  even  when  a  fair  and  accessible  exposure  existed.  Sedation 
for  a  day  or  two  sometimes  permits  a  successful  application.  The 
pressure  is  sometimes  tolerated,  yet  failure  results.  This  action  of 
cocain  corresponds  to  that  in  inflamed  tissue.  Sometimes,  even 
when  the  spunk  enters  the  pulp  tissue,  the  pulp  is  still  sensitive 
higher  up.  In  such  a  case  I  have  often  packed  devitalizing  fiber 
into  the  pulp  in  place  of  the  spunk  and  without  further  pain.  In 
cases  of  cavities  without  walls  to  confine  the  rubber,  it  is  well  to 
enclose  the  buccal  and  lingual  embrasures  with  the  thumb  and 
forefinger.  In  very  broad  occlusal  cavities  the  finger-tip  confines 
the  rubber  nicely. 

When  only  canal  filaments  are  present,  any  septic  matter  present 
should  be  removed  by  syringing  repeatedly  with  an  antiseptic  solu- 
tion; then  the  canals  should  be  thoroughly  dried,  and  the  cocain, 
dissolved  in  an  antiseptic,  is  carried  on  a  cotton  thread  into  the  canals 
and  against  the  pulp  remnant.    A  small  piece  of  rubber  is  placed  in 


ANESTHESIA   OF  THE  PULP  517 

one  canal  and  the  pressure  confined  to  that  canal  by  means  of  a 
plugger  which  will  about  fill  the  canal.  The  action  is  then  repeated 
in  the  other  canals.  This  produces  better  results  than  a  general 
pressure  over  all  the  canals  at  once. 

If  used  after  arsenic  has  been  applied  the  results  are  not  usually  so 
good,  but  sometimes  the  method  is  successful.  To  avoid  the  intro- 
duction of  arsenic  into  apical  tissue  all  sloughing  portions  should  be 
removed  and  all  arsenic  washed  out. 

When  the  pulp  is  not  exposed,  the  application  to  the  dentin  over 
the  pulp  permits  advance,  a  pocket  being  created  in  the  dentin  with 
a  bur,  which  aids  the  further  instillation  of  the  cocain;  finally,  the 
pulp  is  exposed  and  the  anesthesia  is  completed. 

Clyde  Davis  recommends  for  the  purpose  of  producing  the  exposure 
the  use  of  a  drop  of  1  to  1000  adrenalin  chlorid  followed  by  a  drop  of 
37  per  cent,  formaldehyd,  then  pressure  with  raw  vulcanite. 

Where  calcific  formations  are  present  they  present  some  difficulty, 
though  with  persistence  one  may  be  enabled  to  anesthetize  the  pulp. 
Custer  recommends  75°  to  90°  sulphuric  acid  to  aid  in  loosening 
the  nodule.  Cook  recommended  an  application  of  10  per  cent, 
sulphuric  acid  for  a  few  minutes,  followed  by  sodium  bicarbonate 
previous  to  a  reapplication  of  the  pressure  anesthesia,  as  highly 
effective  in  aiding  penetration  of  the  cocain.  Desiccation  is  always 
a  valuable  preliminary,  aiding  penetration.  Claims  are  made  for 
eucain,  or  alcohol  for  producing  pulp  anesthesia  by  pressure. 

There  is  a  possibility  of  the  introduction  of  cocain  into  the  general 
circulation,  and  some  systemic  effect  may  be  noted,  though  often 
this  will  be  due  to  the  agitation  of  the  patient.  Some  patients  have 
complained  of  tingling  in  the  fingers.  If  syncope  be  threatened 
aromatic  spirit  of  ammonia  should  be  administered,  the  head  lowered, 
the  feet  elevated,  and  smelling  salts  or  am}'l  nitrite  applied  to  the 
nostrils.  It  is  always  well  to  administer  aromatic  spirit  of  ammonia 
or  camphorated  validol  before  using  cocain  for  any  purpose. 

Hemorrhage  following  the  extirpation  of  the  pulp  is  sometimes 
copious.  To  avoid  this,  carbolic  acid  should  be  instilled  into  the 
pulp  tissue  by  means  of  a  smooth  broach.  A  fine  Donaldson  cleanser 
may  be  passed  to  the  apex  of  the  canal  and  slowly  twisted,  the  oper- 
ation consuming  several  minutes.  This  torsion  of  the  pulp  largely 
limits  the  hemorrhage.  If  it  occur  it  should  be  allowed  to  check 
itself,  though  if  desired  a  trifle  of  a  mixture  of  powdered  alum  and 
powdered  thymol  may  be  taken  upon  cotton  wet  wdth  phenol- 
camphor  and  passed  to  the  end  of  the  canal.  Deliquesced  zinc  chlorid 
checks  hemorrhage  promptly;  a  dilution  is  less  painful. 

It  is  an  open  question  whether  canals  from  which  living  pulps 


518     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

have  been  removed  should  be  filled  unmediately  or  not.  There  is 
liable  to  be  a  secondary  hemorrhage,  particularly  when  adrenalin 
is  used  with  the  cocain.  Many  prefer  to  fill  at  once,  claiming  that 
surgical  pericementitis  is  the  only  result.  The  writer,  as  a  rule,  wraps 
a  twist  of  cotton  upon  a  Swiss  broach,  dips  it  into  phenol-camphor, 
then  into  formocresol,  and  applies  it  to  the  canal.  This,  as  a  rule, 
permits  the  healing  of  the  parts  without  much  tenderness,  and 
really  consumes  but  little  more  time  in  the  aggregate.  Moreover, 
the  formocresol  tends  to  mummify  the  fibrils  left  in  the  dentinal 
tubules.    " 

All  work  should  be  done  under  aseptic  precautions.  Where  applic- 
able and  not  liable  to  be  too  painful,  the  rubber  dam  should  be 
applied.  The  writer  often  uses  napkins  instead,  and  relies  upon  the 
carbolic  acid  instilled  into  the  pulp  and  the  formocresol  dressing  to 
maintain  asepsis.    This  is  repeated  if  the  cavity  be  douched  out. 

(b)  When  considerable  dentin  overlies  the  pulp,  or  when  a  tooth  is 
sound,  the  most  expeditious  method  of  pulp  anesthesia  is  by  means 
of  the  compound  syringe.  This  consists  of  a  strong  metal  syringe, 
the  piston  of  which  is  actuated  by  means  of  levers  which  multiply 
the  power  of  the  hand.  The  Myers  syringe  is  one  of  the  best, 
'though  several  forms  are  obtainable  (see  Fig.  375).  The  syringe 
nozzle  is  embedded  in  a  small  hole  drilled  in  the  dentin  by  one  of 
two  methods:  The  hole  may  be  made  small  with  parallel  sides,  as 
when  drilled  with  a  No.  |  bur;  the  syringe  nozzle  has  then  slightly 
conical  sides  at  the  point,  intended  to  jam  a  fit  when  introduced  with 
force  into  the  drill  pit.  In  the  other  method  the  drill  pit  is  made 
with  a  cone-pointed  bur  or  bud  bur,  and  the  syringe  point  is  made 
flat-ended,  a  form  easy  to  maintain  upon  the  point.  A  4  to  10  per 
cent,  novocain  solution  is  sufficient,  and  all  air  must  be  expelled 
from  the  syringe.  It  is  wise  also  to  expel  all  air  from  the  drill  pit 
by  a  slight  pressure  while  the  syringe  point  is  loosely  held  in  the  pit. 
Then  a  rotary  motion  under  forward  pressure  embeds  the  point. 

If  no  leakage  occurs  the  force  of  the  piston  drives  the  anesthetic 
through  the  fibrils  in  the  tubules  and  into  the  pulp.  The  pressure 
must  be  maintained  for  about  three  minutes.  The  anesthesia  is 
then  tested  by  drilling  with  a  No.  |  bur  in  the  direction  of  the  pulp. 
If  the  dentin  be  sensitive  the  syringe  is  to  be  reapplied.  Often  the 
bur  sinks  into  a  sensitive  pulp  without  warning  by  dentinal  sensi- 
tivity. In  such  case  the  syringe  is  reapplied  for  a  moment,  when, 
as  a  rule,  the  anesthesia  will  be  complete.  In  all  cases  when  testing 
the  drill  hole  should  not  be  enlarged,  as  this  prevents  reapplication. 
Too  much  cocain  should  not  be  introduced,  as  it  has  happened  that 
the  area  about  the  apical  tissue  has  been  profoundly  injected,  with. 


ANESTHESIA  OF  THE  PULP  519 

of  course,  possibility  of  systemic  complication.  This  warning 
applies  to  the  second  application  rather  than  the  first.  Novocain  is 
less  dangerous.  When  desirable,  the  enamel  of  a  sound  tooth  which  is 
to  be  crowned  may  be  ground  away  until  the  dentin  is  reached,  or 
if  enamel  must  be  removed  in  only  limited  degree,  as  for  a  tap  upon 
the  lingual  side  of  an  incisor  or  in  the  fissure  of  a  bicuspid,  a  "spot" 
is  first  made  with  a  dentate  bur,  then  a  spear  drill  is  driven  through 
the  enamel  only  just  reaching  the  dentin.  The  drill  hole  is  then 
enlarged  as  widely  as  permissible,  after  which  the  pit  is  made  in  the 
dentin  with  a  No.  |  bur. 

The  lingual  side  of  upper  incisors  will  permit  of  sufficiently  direct 
pressure  to  enable  the  operator  to  centre  the  syringe  point,  but  in 
many  cases  in  which  crowns  are  indicated  the  labial  side  may  be 
used  with  advantage,  especially  at  the  neck  when  the  cementum  is 
exposed.  Later,  the  entrance  tap  is  made  in  line  with  the  pulp  axis. 
The  labial  or  mesiobuccal  side  must  always  be  used  in  the  lower  teeth, 
unless  a  cavity  be  used,  sometimes  preferably  at  the  neck,  sometimes 
higher  up.  In  cavities  having  sufficient  dentin  over  the  pulp  the  pit 
may  be  made  in  the  pulpal  wall,  and  if  for  any  reason  it  is  needed 
the  drill  pit  may  begin  at  the  cervical  portion  of  the  cavity  and  extend 
into  the  root  dentin  and  parallel  with  the  pulp.  The  pit  must  be 
deeper  than  the  syringe  point  will  penetrate,  so  that  the  pressure 
may  force  the  solution  laterally  through  the  tubules,  which  are  at 
a  right  angle  to  the  axis  of  the  pulp  and  the  pit.  In  some  cases  solu- 
tions of  antiseptics  have  been  as  effective  with  this  instrument  as 
the  cocain  solution.    The  experiment  may  not  be  successful. 

According  to  Brouardel,^  of  Paris,  the  effects  of  cocain  are  acute 
and  chronic.  The  former  develop  usually  in  ten  or  fifteen  minutes, 
or  even  up  to  three-quarters  of  an  hour  after  the  injection.  They  are : 
precordial  anxiety,  filiform  and  extra  rapid  pulse,  lividity  of  the  face, 
coldness  in  the  extremities,  and  abundant  perspiration;  rise  in  tem- 
perature, irregular  respiration,  tingling  sensations  in  the  hands, 
blunted  tactile  sensibility,  excitement,  loquacity,  weeping,  anger  or 
hysterical  fits;  bilious  vomiting  with  or  without  diarrhea,  anuria, 
symptomatic  epilepsy,  followed  by  motor  and  sensory  paralysis. 
Death  occurs  in  from  two  minutes  to  five  hours  after  administration, 
though  in  the  chronic  cases  fatality  usually  does  not  result. 

Placing  the  patient  in  the  horizontal  position,  give  inhalations 
of  amyl  nitrite,  and,  if  further  cardiac  stimulation  be  necessary, 
hypodermic  injections  of  ether  or  strychnin. 

The  chronic  poisoning  occurs  mostly  in  those  addicted  to  its  use. 

1  Dental  Cosmos,  1905,  p.  1508. 


520      REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

Some  develop  a  tolerance  of  the  drug,  withstanding  from  30  to  120 
grains.  Tachycardia  and  intense  psychic  disturbances,  leading  to 
physical  and  mental  collapse,  are  observed. 

(c)  The  third  and  least  desirable  form  of  cocain  anesthesia  of  the 
pulp  consists  of  its  introduction  by  the  cataphoric  current.  It  has 
the  disadvantage  of  consuming  more  time,  but  may  serve  when 
patients  are  timid.  A  10  per  cent,  solution  of  cocain  hydrochlorid 
is  applied  to  the  pulpal  wall  of  the  cavity,  the  tooth  being  previously 
placed  under  rubber  dam.  The  anode  of  the  cataphoric  outfit  is 
applied  to  the  cotton  and  the  cathode  placed  in  the  hand  or  at  the 
cheek. 

The  dentin  may  be  anesthetized  as  well.  If  desired,  this  method 
may  be  used  to  obtain  a  pulp  exposure  and  the  pressure  method 
employed  to  complete  the  operation. 

When  beginning  with  an  exposed  pulp,  about  fifteen  minutes  will 
be  required  unless  hyperemia  of  the  pulp  exists,  when  a  longer  time 
will  be  required.  As  with  the  pressure  method,  there  may  be  occa- 
sional failures.  It  will  be  noted  that  there  is  advantage  in  time  and 
convenience  in  the  pressure  methods.     (See  p.  403.) 

id)  The  fourth  method  of  producing  pressure  anesthesia  consists  in 
the  use  of  carbolic  acid  in  place  of  the  cocain,  or  in  case  of  obstinate 
canal  filaments  of  a  solution  of  cocain  in  carbolic  acid.    (See  p.  496.) 

(e)  The  fifth  method  of  producing  pulpal  anesthesia  is  by  the 
application  of  nervocidin,  an  alkaloid  obtained  by  D.  Dalma  from 
the  East  Indian  plant  gasu-hasu.  Arkovy  recommended  that  a 
portion  be  applied  to  the  exposed  pulp  for  twenty-four  hours,  when 
it  may  be  removed  painlessly.  Soderberg^  suggests  the  addition  of 
a  small  amount  of  cocain  hydrochlorid  to  overcome  the  primary 
irritating  effect  of  the  nervocidin.  If  dentin  be  over  the  pulp,  an 
additional  application  of  twenty-four  hours'  duration  is  required  to 
obtain  an  exposure.    (See  p.  409.) 

Sprays  of  rapidly  vaporizable  substances,  such  as  ethyl  or  methyl 
chlorid,  directed  against  the  exposed  pulp,  the  tooth  being  isolated 
under  rubber  dam,  will,  in  some  cases,  render  the  pulp  entirely 
insensitive,  although,  as  a  rule,  they  fail  to  entirely  anesthetize  to 
the  apical  foramen.  The  method  is  painful  and  not  applicable  in 
many  cases  of  highly  irritable  pulps.     (See  p.  402.) 

3.  Anesthesia  of  the  Conductive  Apparatus. — The  third  general 
principle  consists  in  the  use  of  mucous,  diploeic  or  conductive 
anesthesia  to  block  the  transmission  through  the  fifth  nerve  leading 
from  the  part.    This  has  been  previously  described  for  hypersensitive 

1  Dental  Cosmos,  1901  and  1902. 


DEVITALIZATION  OF  THE  PULP  521 

dentin  (see  page  407) .  Claims  have  been  made  for  a  slight  sidewise 
blow  struck  upon  the  tooth  to  paralyze  the  pulp  nerves  by  a  stretch- 
ing shock. 

4.  Devitalization  of  the  Pulp. — Devitalization  of  the  pulp  by  the 
use  of  arsenic  trioxid  as  a  preliminary  to  its  successful  removal 
is  the  oldest  of  the  methods  employed  at  the  present  day/  and 
as  shown,  it  still  has  to  be  resorted  to  either  from  necessity  or 
convenience. 

The  method  has  its  value  in  the  very  teeth  in  which  its  use  is  least 
objectionable,  namely,  the  posterior  teeth.  There  is  no  danger  of 
the  use  of  arsenic  in  teeth  having  completed  roots,  or  in  unresorbed 
temporary  teeth,  provided  the  arsenic  be  accurately  sealed  in  the 
cavity  so  that  it  does  not  escape  upon  the  gum.  If  it  does  escape  it 
may  destroy  the  gum  or  pericementum  and  cause  partial  necrosis  of 
bone  or  the  complete  loss  of  the  tooth  together  with  some  bone.  The 
pulp  always  dies  through  a  process  of  venous  hyperemia  induced  by 
the  protoplasmic  irritant  and  poison.  Some  of  this  is  absorbed  by 
the  pulp.  This  hyperemia  is  progressive  from  the  pulp  bulb  toward 
the  apex  of  the  root,  and  there  it  causes  the  death  of  the  apical  portion 
of  pulp  through  interference  with  its  nutrition.  Sometimes  this 
hyperemia  of  the  pulp  extends  into  the  apical  tissue,  but  if  the  pulp 
be  left  in  situ,  necrosis  of  apical  tissue  never  results,  but,  on  the 
contrary,  the  hyperemia  becomes  resolved  after  the  death  of  the 

pulp. 

The  writer  fails  to  see  wherein  such  a  hyperemia  differs  in  conse- 
quence from  that  produced  by  the  surgical  removal  of  a  pulp  and 
denominated  with  favor  as  surgical  pericementitis.  In  his  hands 
such  teeth  have  given  quite  as  good  results  as  when  other  methods 
have  been  employed.  By  this  it  is  not  meant  that  there  has  been 
no  difficulty  in  devitalizing  some  pulps,  particularly  some  of  those 
in  which  repeated  applications  of  cocain  under  pressure  failed  to 
anesthetize,  but  that  when  carefully  handled  and  sufficient  time  for 
pulp  death  has  been  allowed,  careful  filling  of  the  canal  has  been 
successful. 

Action  of  Arsenic  upon  the  Pulp. — Arkovy^  was  the  first  to  point 
out  the  details  of  the  action  of  arsenic  upon  the  dental  tissues : 

"1.  AS2O3  brought  into  contact  with  the  tooth  pulp  acts  in  the 
following  way :  A  certain  degree  of  inflammatory  hyperemia,  total  or 
partial,  depending  upon  the  quantity  of  the  agent  applied,  sets  in; 
the  bloodvessels  become  expanded,  and  here  have  a  tendency  to 
thrombosis.     This  latter   effect  may   also   be   in   connection   with 

1  Introduced  by  Spooner  in  1836. 

2  Transactions  of  the  International  Medical  Congress,  London,  1881. 


522     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL   FILLING 

embolism  of  the  capillaries,  when  the  agent  is  quickly  taken  up  into 
the  bloodvessels. 

"2.  AS2O3  produces  no  coagulation  of  tissue  whatever. 

"3.  It  has  a  specific  influence  upon  the  blood  corpuscles,  combining 
with  the  hemoglobin  to  form  a  compound  of  arsen-hemoglobin,  and 
of  this  chemical  process  there  seems  to  be  evidence  in  the  profuse 
yellowish  tinge  of  the  whole  pulp  tissue  and  in  the  discoloration  of 
blood  in  several  of  the  bloodvessels. 

"4.  In  nearly  every  case  it  is  taken  up  in  substantia  (in  form  of 
molecules)  into  the  blood-ways;  when  there  it  produces  besides  the 
above-mentioned  changes,  granular  detritus  of  the  contents  and 
anemic  collapse — shrinkage,  the  latter  effect  being  brought  about 
nearly  exclusively  in  cases  where  greater  doses  were  used. 

"5.  The  bulk  of  the  pulp  tissue — viz.,  connective-tissue  fibers  and 
odontoblasts — undergoes  no  change  whatever;  not  so  the  connective 
tissue  cells,  which  increase  three  or  four  times  their  normal  size.     • 

"6.  The  special  action  of  arsenic  trioxid  upon  the  nerve  element 
consists  in  the  following:  the  neurilemma  is  only  so  far  influenced 
that  its  nuclei  are  somewhat  increased;  a  more  essential  change  takes 
place  in  the  axial  part,  where,  after  the  application  of  more  than 
1  mg.,  granular  destruction  of  myelin  sets  in,  and  the  axis-cylinder 
commences  here  and  there  to  disappear.  A  very  surprising  alteration 
may  be  seen  in  the  notchy  tumefaction  of  the  axis-cylinder,  described 
heretofore  almost  only  in  cases  of  central  lesions. 

"7.  All  these  alterations  occur  in  and  among  normal-looking  tissue. 

"8.  The  action  of  arsenic  trioxid  is  macroscopically  exhibited  by 
a  brownish-red  tinging  of  the  whole  or  of  certain  parts  of  the  pulp 
body,  as  well  as  of  the  neighboring  dentin  and  the  cementum,  this 
latter  in  cases  treated  with  greater  doses — viz.,  2  to  5  mg.  This 
alteration  is  most  expressed  at  the  top  of  the  crown  pulp  and  at 
the  apical  one-fourth  to  one-third  part.  This  circumstance  may 
be  considered  as  an  external  evidence  of  the  devitalization  being 
completely  attained  to." 

In  some  cases  the  pinkish  discoloration  of  the  dentin  may  be 
marked;  the  broken-down  corpuscles  of  the  extravasated  blood  have 
their  coloring  matter  taken  up  by  the  odontoblasts,  and  being  dis- 
tributed through  their  protoplasmic  processes  produce  a  condition 
technically  known  as  suffusion.  The  same  result  may  be  an  attendant 
upon  injury  to  the  vessels  from  other  causes,  producing  hyperemia, 
as  when  teeth  are  moved  too  rapidly  in  regulating.     (See  p.  480.) 

Miller's  experiments^  upon  the  tails  of  mice  (made  without  and 

1  Dental  Cosmos,  1894. 


DEVITALIZATION  OF  THE  PULP  523 

with  rings  at  the  root  of  the  tail  to  simulate  the  surrounding  of  the 
apical  vessels  of  a  tooth;  made  without  and  with  encasement  of  the 
tails  in  plaster  of  Paris  to  imitate  the  rigid  surroundings  of  the  dental 
pulp)  showed  that  in  the  absence  of  the  plaster  encasement  enormous 
edema  of  the  tail  was  produced  and  a  sensory  paralj^sis  of  the  hind 
limbs;  complete  anesthesia  of  the  tail  occurred  in  forty-eight  hours. 
"  The  action  of  arsenic  appeared  somewhat  accelerated  when  a  glass 
ring  was  applied  close  to  the  root  of  the  tail.  In  more  than  forty  cases 
there  was  not  one  in  which  the  action  of  the  arsenic  extended  beyond 
the  ring,  and  the  action  was  not  appreciably  affected  by  enclosing  the 
tails  in  plaster  casts.  The  action  of  the  arsenic  is  of  a  progressive 
nature,  beginning  at  the  point  of  application  and  extending  gradually 
in  each  direction." 

Flagg'^  devitalized  ten  pulps  and  removed  them,  cut  off  the  portion 
of  the  bulb  of  each  which  had  contact  with  the  arsenic,  and  tested  the 
ten  pulps  together  by  Reinsch's  test.  Arsenic  was  found,  estimated 
at  a  one-hundred-thousandth  part  of  a  grain,  or  one-millionth  of  a 
grain  for  each  pulp.  Allowing  for  possible  mechanical  introduction 
or  contact  of  arsenic  during  extirpation,  the  quantity  of  arsenic 
introduced  by  the  circulation  must  be  very  minute  indeed. 

Flagg  argued  that  as  the  pulp  subsequently  putrefies  it  cannot 
have  died  as  the  result  of  arsenical  poisoning  alone. 

In  the  roots  with  large  foramina  arsenic  may  be  absorbed,  as  areas 
of  devitalization  of  the  apical  and  overlying  gum  tissue  have  been 
noted.  In  several  apparently  authentic  cases  the  pericementum  of 
a  mature  tooth  has  been  said  to  be  destroyed  from  the  apex  down 
and  the  tooth  lost.  I  have  never  seen  such  a  case  resulting  from  the 
arsenical  method  alone  in  either  clinical  or  private  practice,  although 
cases  of  marginal  gum,  alveolar,  and  pericemental  death,  beginning 
as  the  result  of  leakage  or  application  to  perforations,  have  been 
noted.  It  is  probable  that  as  stasis  proceeds  the  apical  portion  of 
the  pulp  becomes  involved  in  advance  of  arsenic  absorption.  Miller's 
experiments  show  that  arsenic  does  not  pass  the  point  of  constriction. 

Variations  in  the  Action  of  Arsenic. — In  most  cases  of  fully  formed, 
single-rooted  teeth  in  young  adults  an  application  of  arsenical  paste 
directly  to  the  exposed  pulp  will  be  followed  by  the  complete  death 
of  the  organ  in  forty-eight  hours.  At  the  expiration  of  that  time  a 
sterilized  broach  may  be  passed  almost  to  the  apex  of  the  root  and 
the  pulp  removed  en  masse  without  pain.  Pulps  of  molars  require  a 
longer  time,  often  a  week,  before  the  filaments  are  dead.  The  finer 
filaments  resist  longer  than  the  larger  ones.     If  pulp  nodules  exist, 

1  Dental  Cosmos,  1868. 


524     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL   FILLING 

the  action  of  the  arsenic  may  be  delayed  or  in  some  cases  be  almost 
nil.  In  calcareous  and  other  chronic  pulp  degenerations  the  action 
is  also  delayed.  If  arsenical  applications  are  made  over  a  layer  of 
dentin,  the  same  delay  is  noted,  and  is  increased  in  very  dense 
teeth.    There  is  also  a  greater  tendency  to  suffusion. 

Some  pulp,  irrespective  of  the  pulp  condition,  exhibits  a  peculiar 
idiosyncrasy  in  resisting  the  action  of  arsenic,  requiring  large  doses 
and  long  applications  before  succumbing.  Second  applications  often 
require  more  time  to  kill  the  balance  of  the  pulp  than  the  first  appli- 
cation would  have  required.  The  time  used  in  investigation  is 
practically  lost.  The  editor,  therefore,  allows  plenty  of  time;  about 
ten  days  for  molars,  five  for  single-rooted  teeth,  and  prefers  to  find 
the  pulp  entirely  dead. 

The  rational  objections  to  arsenic,  aside  from  its  escape  upon  the 
gum,  are:  (1)  The  possible  production  of  pain.  (2)  Possible  suffu- 
sion of  the  tooth.     (3)  The  time  required. 

The  production  of  pain  may  largely  be  obviated  by  observance  of 
certain  technique.  The  pulp  should  ordinarily  be  exposed  and  be 
slightly  bled  to  relieve  any  hyperemia  or  inflammatory  engorgement 
present,  as  this  seems  to  prevent  the  absorption  of  the  arsenic,  A 
powerful  sedative,  such  as  thymol,  menthol,  cocain  hydrochlorid 
or  morphin  acetate,  should  be  employed  as  a  corrective,  and  the 
menstruum  should  be  sedative  rather  than  coagulant.  All  pressure 
on  the  pulp  should  be  avoided  as  this  produces  pain. 

Sufficient  time  for  complete  death  should  be  allowed,  say,  from  a 
week  to  ten  days.  If,  upon  examination  with  a  fine  smooth  broach, 
vitality  be  discovered,  a  sedative  should  be  applied  and  pulp  death 
awaited.  Leaving  the  dead  portion  against  the  vital  part  of  the  pulp 
is  even  better  than  making  a  second  application,  as  its  removal 
relieves  the  congestion  by  opening  the  vessels,  and  the  congestion  is 
necessary  to  the  end  in  view.  If  the  pulp  give  but  little  response 
upon  probing  it  may  be  removed.  Sometimes  the  diapedesis  of  red 
corpuscles,  associated  with  the  venous  hyperemia,  causes  a  staining 
of  the  pulp  and  dentinal  fibrils  with  the  liberated  hemoglobin.  This 
is  unfortunate,  but  can  be  treated  by  bleaching  with  25  per  cent, 
ethereal  pyrozone  sealed  in  the  pulp  cavity  for  about  twenty-four 
hours  after  the  pulp  is  removed.  The  third  objection,  the  matter 
of  time,  does  not  apply  to  the  cases  of  prompt  devitalization,  as  the 
time  spent  in  pulpal  anesthesia  and  checking  hemorrhage  is  in  the 
aggregate  no  less  than  in  the  arsenical  cases.  In  the  delayed  action 
of  arsenic  the  objection  is  valid,  but  the  conductive  and  general 
anesthesia  methods  are  still  open  to  trial.  The  arsenical  method,  of 
course,  requires  a  longer  period  of  treatment.     Pulpal  anesthesia 


DEVITALIZATION  OF  THE  PULP  525 

can  be  tried  when  arsenic  does  not  act  well,  but  should  be  avoided 
when  it  originally  failed.  Mucous,  diploeic  and  conductive  anesthesia, 
or  general  anesthesia  may  be'  used  if  arsenic  fails.  As  stated,  these 
considerations  apply  mainly  to  posterior  teeth. 

Forms  in  Which  Used. — The  following  is  an  excellent  formula  for 
arsenical  paste: 

I^ — Arsenici  trioxidi       . gr.  xv 

Cocainse  hydrochloridi gr.  xx 

Thymolis  (vel  mentholis) gr.  v 

Olei  caryophyili q.  s.  ft.  pasta — M. 

This  should  be  finely  ground  in  a  mortar  and  spread  over  the  bottom  of  a  wide  glass 
jar  so  that  some  of  the  paste  may  be  taken  up  from  the  bottom.  The  arsenic  settles 
to  the  bottom. 

Buckley  recommends  the  following  formula: 

IJ — Arsenic  trioxid gr.  clxxx 

Cocain  alkaloid gr.  xxx 

Thymol gr.  xv 

Petronal lUxv — M. 

Either  of  the  above  may  have  the  powdered  ingredients  mixed. 
The  cotton  pellet  may  be  wet  with  the  menstruum  and  then  dipped 
into  the  powder.  Lamp  black  added  to  the  paste  colors  it  so  that  it 
is  easily  distinguishable  in  a  cavity. 

Prinz  has  suggested  the  rational  improvement  of  using  a  con- 
centrated solution  of  cocain  or  novocain  before  applying  arsenic. 
This  renders  its  primary  action  less  painful,  or  painless.^ 

The  following  are  other  formulae:  The  analgesics  included  are 
intended  to  dilute  the  arsenic  and  quiet  the  pulp,  and  thus  both 
directly  and  indirectly  modify  the  pain. 

I^ — Acidi  arsenosi, 

Morphinse  sulph aa  gr.  x 

Acidi  carbolici .      q.  s.  ft.  pasta — M. 

(J.  D.  White.) 

I^ — Acidi  arsenosi gr.  x 

Morphinse  acetatis gr.  xx 

Olei  caryophyili q.  s.  ft.  pasta — M. 

(J.  Foster  Flagg.) 
Creosote  may  be  substituted  for  oil  of  cloves. 

I^ — Acidi  arsenosi gr.  x 

Cocainse  hydroch gr.  xx 

Olei  cinnamomi        .      . q.  s.  ft.  pasta — M. 

(E.  C.  Kirk.) 

I^ — Arsenic gr.  x 

Alum .       .       .  gr.  X 

Thymol gr.  x 

Oil  of  cloves i .      .      .      .  q.  s.  ft.  pasta— M. 

1  Dental  Materia  Medica  and  Therapeutics. 


526     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

As  the  ordinary  pastes  tend  to  separate  into  layers  of  arsenic, 
morphin,  etc.,  and  menstruum  if  made  thin,  they  should  either  be 
made  into  stiff  pastes  or  spread  over  the  bottom  of  a  wide  jar,  so  that 
some  arsenic  may  be  scraped  off  the  bottom  at  each  application. 

W.  H.  Truman  indorses  the  opinion  of  J.  D.  White  that 
thorough  trituration  for  two  hours  more  finely  divides  the  arsenic 
and  prevents  separation,  and  claims  that  the  use  of  arsenic 
triturated  with  wood  creosote  and  glycerin  is  the  most  effective 
preparation.^ 

Miller  offers  the  following  general  rules  as  deductions  from  his 
observations : 

"1.  The  rapidity  and  intensity  of  the  action  of  arsenous  acid 
depend,  under  certain  circumstances,  to  a  very  considerable  degree 
upon  the  substance  or  substances  with  which  it  is  incorporated. 

"2.  Where  there  is  but  a  small  point  of  exposure,  arid  in  particular 
where  extensive  calcification  has  taken  place  in  the  pulp,  escharotics 
should  be  avoided,  since  the  coagulation  of  the  tissue  retards  the 
absorption  of  the  arsenic.  This  retardation  is  but  slight  where  there 
is  a  broad  surface  of  exposure.  In  stubborn  cases,  where  applica- 
tions of  the  ordinary  paste  fail  to  effect  the  devitalization,  a  paste 
consisting  of  arsenous  acid  in  oil  of  cloves,  glycerin,  or  salt  solution 
should  be  employed,  undiluted  by  any  third  constituent. 

"3.  Thymol  is  worthy  of  a  trial  as  a  substitute  for  morphin,  on 
account  of  its  anesthetic  and  antiseptic  properties. 

"4.  For  devitalizing  pulps  of  temporary  teeth  or  remains  of  pulp 
tissue  in  root  canals,  arsenous  acid,  if  employed  at  all,  should  be 
diluted  with  two  or  three  parts  of  some  other  constituent  (thymol, 
zinc,  oxid,  morphin,  iodoform)." 

Cobalt  was  introduced  by  Robert  Arthur  as  a  devitalizing  agent 
some  forty  years  ago.  Within  recent  years  it  has  been  employed, 
notably  by  the  Herbst  method,  to  destroy  pulps.  The  cobalt  paste 
of  Herbst  was  analyzed  by  E.  C.  Kirk,  and  found  to  consist  of 
metallic  arsenic  and  cocain  hydrochlorid.  Kirk  suggests  that  free 
acids  which  cocain  salts  may  contain,  or  the  chlorin  from  the  chlorid, 
may  combine  with  the  metallic  arsenic  and  form  soluble  salts.  The 
use  of  arsenic  pentoxid  and  soluble  arsenates  has  been  suggested  by 
Fette,  and  for  which  he  claims  advantages.^ 

There  are  some  advantages  in  the  so-called  devitalizing  fiber 
introduced  by  J.  Foster  Flagg.  To  make  this,  absorbent  cotton  is 
cross-cut  with  scissors  to  a  fine  lint.  This  is  dusted  into  the  paste 
or  ground  up  with  it  in  the  mortar.    It  may  then  be  dried  on  a  blotter 

1  Dental  Brief,  June,  1913.  2  Dental  Cosmos,  November,  1914. 


DEVITALIZATION  OF  THE  PULP 


527 


Fig.  453 


and  be  bottled  for  use.  As  it  lacks  long  fibers,  a  small  portion  may  be 
detached  and  be  placed  upon  the  pulp.  There  are  cases,  however, 
in  which  the  paste  should  be  carried  to  the  exposure  upon  a  probe 
and  gently  inducted  into  a  fine  exposure.  Here  its  tendency  to  spread 
or  penetrate  is  valuable.  The  fiber  has  no  such  tendency,  which 
makes  it  less  dangerous  in  use.  In  making  the  application  a  minute 
portion  of  paste  is  to  be  laid  upon  the  pulp,  or  a  pin-head  pellet  of 
cotton  is  rolled  in  it,  the  excess  of  menstruum  removed,  and  it  is 
then  applied  to  the  pulp,  or  a  portion  of  devitalizing  fiber  is  used. 
This  is  then  sealed  in. 

The  cavity  should  be  prepared  for  the  reception  of  arsenic,  decay 
being  removed  as  far  as  practicable,  and  the  cavity  dried.     Any 
redundant  gum  must  be  pressed  away  or 
saturated  with   trichloracetic   acid    and 
ablated. 

There  are  two  good  methods  of  seal- 
ing the  arsenic.  In  cases  not  approach- 
ing the  gum,  or  where  dryness  can  be 
maintained,  the  application  may  be 
accurately  made  and  quick-setting  cement 
flowed  over  it.  This  cement  is  capable 
of  being  fairly  dropped  into  a  cavity  or 
led  around  the  periphery  by  a  probe,  and 
should  be  very  adhesive,  also  be  readily 
removable.  A  still  safer  method  consists 
in  applying  a  pellet  of  amadou  over  a 
part  of  the  pulpal  wall.  The  cement  is 
then  introduced  about  the  periphery  of 
the  cavity,  the  amadou  being  left  largely 

uncovered.  When  hard,  any  cement  over  the  amadou  is  removed 
and  the  latter  lifted  out,  thus  leaving  a  box-like  receptacle  for 
the  arsenic  and  a  pellet  of  amadou  partly  wet  with  eugenol  in 
which  menthol  is  dissolved.  When  placed,  the  orifice  is  dried  and 
more  cement  added.  This  method  of  first  making  the  covering  is 
of  special  advantage  when  the  cavity  cervix  is  near  the  gum,  and  pre- 
vents the  forcing  of  arsenic  toward  the  gum  in  the  act  of  making  the 
covering.  Amalgam  or  facing  amalgam^  .or  temporary  stopping 
may  be  used  in  place  of  the  cement  (Fig.  453).  Temporary  stopping 
is  not  very  safe  against  masticatory  force. 

The  rubber  dam  is  generally  insisted  upon,  but  cannot  be  used  in 
the  worst  cases,  hence  an  expert  may  dispense  with  it.    There  is  a 


Diagram  showing  method  of 
first  making  the  covering  for 
an  arsenical  or  sedative  appli- 
cation. (See  text.)  EP,  ex- 
posed pulp;  A  A,  arsenical  ap- 
plication; C,  sedative  covering 
to  same;  A,  amalgarn  placed 
before  these  applications;  A', 
amalgam  to  seal  them  in;  E, 
enamel. 


*  Facing  amalgam  is  silver  40,  tin  55,  zinc  5  parts,  and  mercury. 


528     REMOVAL  OF  DENTAL  PULP  AND    ROOT-CANAL   FILLING 

tendency  among  students  to  rely  upon  the  rubber  dam  alone  to 
prevent  accidents.  This  is  a  fallacy,  as  the  same  results  may  occur 
with  it  as  well  as  without  it.  The  chief  danger  lies  in  the  use  of 
temporary  stopping  after  placing  paste.  Capillarity  and  pressure 
often  carry  the  paste  to  the  cervical  margin.  Making  the  covering 
first  or  using  fiber  constitute  the  best  precautions. 

In  case  of  a  very  dangerous  cavity,  as  a  distocervical  one,  a  special 
drill  pit  known  as  a  "pocket"  is  to  be  made  at  some  other  point 
extending  in  the  direction  of  the  pulp  horn  and  as  near  to  it  as  can 
be  made  without  too  much  infliction  of  pain.  In  this  the  arsenic  is 
to  be  sealed  while  antiseptic  sedatives  are  to  be  placed  on  cotton  in 
the  cavity  of  decay.  This  method  is  also  valuable  when  the  pulp  is 
very  irritable,  and  permits  devitalization  through  a  more  or  less 
healthy  portion  of  pulp. 

The  presence  of  pulp  nodules  may  necessitate  an  application  after 
lifting  away  the  nodule  (Fig.  404) . 

The  arsenical  method  may  be  used  after  a  preliminary  general 
anesthesia  and  bulb  removal,  or  may  even  be  used  against  an  obdurate 
pulp  canal  filament.  When  pulp  removal  is  intended  the  application 
may  be  removed  through  the  opening  and  a  probe  may  be  passed 
into  the  pulp  to  test  the  progress  of  the  devitalization.  If  needed, 
a  second  application  may  be  made  or  the  tooth  may  be  temporarily 
closed.  In  case  the  pulp  be  found  partially  dead,  it  is  better  to 
allow  more  time  for  complete  devitalization  than  to  make  a  second 
application,  as  removing  a  portion  relieves  the  congestion. 

Symptoms. — The  large  majority  of  pulps  die  under  arsenic  with 
but  little  pain.  Sometimes  throbbing  pain  results,  passing  into  a 
heavy  fulness  as  congestion  supervenes.  If  too  great,  the  pulp  should 
be  uncovered  and  bled  slightly,  then  a  sedative  should  be  applied, 
iodin  used  as  a  counterirritant  upon  the  gum,  and  pulp  death  awaited. 
Ordinarily  the  pain  passes  away  as  the  pulp  becomes  more  fully 
congested.  Apical  irritation  may  result  and  may  be  ignored  if  slight, 
or  if  severe  be  treated  in  the  same  way  as  the  pulp  irritation  (Fig. 
412) .  A  guard  to  prevent  overocclusion  is  sometimes  useful  (Fig.  549) . 

Accidents  from  Arsenical  Applications. — If  a  portion  of  an  arsenical 
application  escape  from  beneath  its  covering,  it  may  destroy  much 
or  a  little  gum  tissue,  according  to  the  amount  which  escapes.  The 
teeth  should  be  seen  early  in  doubtful  cases  and  the  condition  of 
the  gum  observed. 

The  arsenic  may  attack  the  gum  festoon,  inducing  in  it  stasis 
followed  by  necrosis.  The  gum  assumes  a  purplish  turgidity,  which 
later  changes  to  a  dirty  yellow  slough. 

The  bone  is  usually  devitalized  for  a  distance. 


DEVITALIZATION  OF  THE  PULP  529 

If  the  necrosis  be  self-limited,  as  is  usually  the  case,  a  small 
sequestrum  comes  away  after  a  few  weeks. 

In  some  cases  the  arsenic  may  follow  the  festoon  of  the  gum  of 
one  or  more  teeth,  causing  disagreeable  sloughs  and  ulcerations. 
It  may  follow  the  pericemental  tract,  kill  the  pericementum,  and  the 
tooth  drops  out.  In  one  case  of  a  boy,  aged  twelve  years,  an  appli- 
cation was  made  in  a  first  lower  molar.  A  blow  from  a  base-ball 
was  subsequently  received  and  a  slight  leakage  occurred  merely  a 
trifling  slough  of  the  gum  being  apparent  mesially.  Later  the 
living  gum  margin  appeared  flabby  and  could  be  lifted  away.  Finally 
and  gradually,  during  nine  months,  the  buccal  pocket  deepened 
without  loss  of  the  gum,  the  tooth  gradually  loosened,  the  bone 
septum  between  the  roots  was  found  necrosed,  the  tooth  was  removed, 
and  the  socket  healed  without  further  necrosis.  The  alveolar  process 
about  one  or  several  teeth  may  be  devitalized  and  a  sequestrum 
occur  which  includes  the  teeth.  .  Certain  toothache  nostrums  are 
sold  which  contain  arsenic.  Dr.  G.  C.  Chance^  records  a  case  of 
arsenical  necrosis  occurring  from  this  source.  Dr.  J.  E.  Pow^ers^ 
records  a  case  in  which  extensive  necrosis  occurred  from  the  use 
of  colored  woolen  yarn  (as  a  cleanser  of  interdental  spaces)  which 
contained  arsenic  used  in  the  dye. 

From  the  infirmary  of  the  Philadelphia  Dental  College  was  re- 
ferred to  the  oral  clinic  a  case  of  extensive  coagulation  necrosis, 
resulting  from  the  rubbing  of  "toothache  drops"  upon  the  gum. 
Analysis  showed  the  preparation  used  contained  arsenic.  Collapse 
from  blood  poisoning  being  the  immediate  danger,  the  child  was 
operated  upon  by  Prof.  Boenning  for  drainage  of  the  parts.  During 
the  recovery,  the  teeth  from  the  right  lower  cuspid  to  the  left  lower 
second  temporary  molar,  and  the  gums  over  the  process,  were  lost, 
leaving  a  blackened  alveolar  process,  to  be  later  removed  surgically 
(Fig.  454). 

Arsenic  is  liable  to  pass  through  the  apical  foramina  of  unformed 
or  much  resorbed  roots.  It  may  possibly  pass  through  mature  roots 
when  an  application  is  placed  high  up  in  the  canal,  rarely  when  applied 
under  normal  conditions  (as  recorded  by  some),  or,  as  occurred  in 
one  case,  by  the  application  being  pushed  through  the  apex.  It 
may  be  forced  through  in  the  act  of  broaching,  or  through  the  sub- 
sequent use  of  the  cataphoric  current  or  pressure  anesthesia  without 
the  preliminary  precaution  of  removing  the  arsenic. 

In  some  cases  arsenic  has  been  applied  to  perforations  made 
through  the  sides  of  roots  under  the  impression  that  the  vital  tissue 

1  Proceedings  of  the  Academy  of  Stomatology,  Philadelphia,  1898. 
-  International  Dental  Journal,  November,  1902. 
34 


530      REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

found  was  pulp  tissue.  In  such  case  its  necrotic  effects  will  be  noted 
upon  the  gum  overlying  the  root  apex  or  over  the  perforation,  the 
tooth  being  loosened  and  extruded  and  may  possibly  be  lost. 

E.  C.  Kirk^  has  recorded  several  cases  of  loss  of  teeth  from  arsenical 
necrosis  of  the  pericemental  tissue  following  the  use  of  mummifying 
paste  to  pulp  stumps  previously  impregnated  with  arsenic.  His 
theory  is  that  the  arsenic  was  liberated  by  the  affinity  of  the  ingre- 
dients of  the  mummifying  paste  for  the  proteid  constituents  of  the 
pulp  tissue.  The  editor  has  often  used  such  pastes  after  arsenic  and 
without  untoward  results,  and  feels  that  some  other  element  must 
have  entered  in  Kirk's  cases. 


Boenning's  case  of  coagulation  necrosis  due  to  arsenic;  shows  exposed  and  blackened 

alveolar  process. 


Such  dangers  as  these  demand  that  extreme  precautions  be  taken 
against  the  careless  use  of  quantities  of  the  agent.  The  rules  laid 
down  should  be  adhered  to. 

The  only  cure  of  the  condition  consists  in  the  thorough  removal  of 
every  particle  of  the  arsenic.  Any  projecting  masses  of  edematous 
gum  should  be  cut  away,  as  they  are  dead  and  will  slough  at  any 
rate,  and  a  freer  access  to  deep  parts  is  had — the  blood-flow  may 
itself  wash  away  the  arsenic.  The  forcible  washing  should  be  pro- 
longed and  repeated,  or  10  per  cent,  silver  nitrate  should  be  used  to 
form  arsenite.  Dialyzed  iron  or  tincture  of  iodin  might  be  applied 
with  a  view  to  possible  neutralization  of  the  arsenic. 

The  editor,  in  a  case  of  known  application  of  arsenic  to  an  obscure 

1  Dental  Cosmos,  October,  1903. 


SPECIAL  METHODS  OF  PREPARING  PULPS  FOR  REMOVAL     531 

perforation,  succeeded  in  causing  regeneration  of  tissue  by  removing 
surgically  the  dead  tissue  and  inviting  repair. 

It  may,  therefore,  be  that  after  minute  portions  of  arsenic,  forced 
through  foramina,  exert  their  full  effect,  the  resulting  dead  tissue 
may  be  removed  by  resorption  or  even  exfoliation;  indeed,  this  result 
has  been  noted  in  which  no  other  explanation  seemed  possible. 

If  the  teeth  are  loosened  and  lost  as  the  result  of  arsenical  necrosis, 
either  beginning  at  the  gum  margin  or  at  the  apical  space,  the  alveolus 
will  exhibit  a  bare  periphery  and  even  some  odor  of  putrefaction  may 
be  present.  The  alveolus  should  be  sterilized  and  the  walls  burred 
away  to  a  tissue  capable  of  healthy  granulation. 

If  suffusion  occur,  essential  oils  or  phenol  should  be  avoided  in  the 
subsequent  treatment,  as  they  tend  to  set  the  color  by  acting  as  a 
mordant  (Kirk),  rendering  bleaching  difficult.  After  the  pulp  is 
removed  it  is  well  to  fill  the  apical  portion  of  the  canal,  and  then 
at  once  bleach  with  25  per  cent,  ethereal  pyrozone,  after  which 
the  balance  of  the  canal  and  the  cavity  may  be  filled.  (See  Moist 
Gangrene  of  the  Pulp,  p.  580.) 

Special  Methods  of  Preparing  Pulps  for  Removal. — A  fully  exposed 
pulp  in  a  single-rooted  tooth  or  single  root  of  a  multirooted  tooth, 
may  be  suddenly  "knocked  out"  by  means  of  a  delicately  pointed 
orange-wood  stick  or  Portuguese  toothpick.  The  point  is  dipped  in 
carbolic  acid  and  suddenly  and  boldly  driven  into  the  pulp,  either  by 
hand  or  mallet  force.  The  method  is  not  so  agreeably  delicate  as 
pressure  anesthesia,  but  is  effective.  It  must  not  be  used  in  partial 
exposure,  as,  not  reaching  the  apex,  it  may  cause  pain.  Its  use  is 
only  indicated  in  emergency  or  occasionally  in  crown  work  after 
excision  of  the  crown  by  excising  forceps. 

A  vital  remnant  of  pulp  may  be  removed  after  instilling  a  strong 
cocain  solution,  or  carbolic  acid,  or  a  paste  of  carbolic  acid  and 
acetate  of  morphin,  into  its  substance  by  means  of  a  "puncture 
probe."  This  instrument  may  be  made  by  filing  down  a  Donaldson 
bristle  to  a  fine  point,  which  is  further  whetted  on  an  oil  stone.  The 
sides  of  the  probe  are  polished  by  folding  a  cuttle-fish  disk  upon 
itself,  holding  it  between  the  thumb  and  forefinger  of  the  left  hand, 
and  drawing  the  probe  through  it.  The  pulp  canal  is  flooded  with 
the  carbolic  acid,  and  gentle  thrusts  are  made  into  the  pulp  until  the 
probe  is  stopped  at  the  apex.  If  it  pass  through,  that  must  be  judged 
by  the  sense  of  touch.  Custer  recommends  75  to  90  per  cent,  sul- 
phuric acid  as  superior  to  carbolic  acid.  At  times  a  small  end  of 
pulp  filament  may  be  seared  with  a  hot  Evans'  root  drier,  which  is 
quickly  thrust  into  it.    This  does  not  necessarily  give  much  pain. 

A  slow  but  effective  method  of  disposing  of  these  filaments,  when 


532     REMOVAL  OF  DENTAL  PULP  AND    ROOT-CANAL  FILLING 

hyperirritable  or  when  patients  are  timid,  consists  in  packing  a 
cotton  twist  saturated  with  carbolic  acid  containing  cocain  hydro- 
chlorate  in  solution  into  contact  with  the  pulp,  and  then  gently 
compressing  the  pulp.  The  cotton  is  to  be  left  in  position  for  a  day 
or  two,  when,  as  a  rule,  the  pulp  may  be  removed.  It  induces  throm- 
bosis, and  carbolic  acid  may  be  used  with  pressure  to  produce 
anesthesia  at  the  time  of  operation.  A  dressing  of  tincture  of  iodin 
has  been  suggested  for  the  purpose. 

Devitalization  of  Pulps  in  Temporary  Teeth. — All  of  the  anesthetic 
measures  are  as  applicable  to  temporary  teeth  as  to  the  permanent 
ones  if  the  little  patient  will  tolerate  their  application. 

If  the  child  present  an  exposed  pulp  in  a  tooth  the  roots  of  which 
are  not  resorbed,  arsenic  much  diluted,  may  be  applied  for  twenty- 
four  hours  and  then  be  removed,  the  pulp  being  then  allowed  to  die. 
When  roots  are  resorbed  it  is  better  to  cap  the  pulp  with  Jodo- 
Formagen  cement,  or  if  necessary,  apply  a  pellet  of  cotton  wet  with 
phenol,  then  touched  to  iodoform,  and  seal  in  with  temporary 
stopping,  making  a  slight  pressure.  This  may  remain  a  week  or 
more  and  be  renewed  if  necessary. 

Darby  has  used  cantharides,  2V  grain  in  carbolic  acid,  with  success. 
It  must  be  carefully  sealed,  as  strangury  is  a  possibility.^  Figs.  146 
and  116  are  guides  as  to  the  condition  of  the  end  of  the  root. 

THE   EXTIRPATION    OF   THE   PULP. 

After  the  pulp  is  prepared  for  removal  or  the  patient  is  anesthe- 
tized, free  access  to  all  parts  of  the  pulp  cavity  and  canals  must  be 
obtained.  This  is  usually  best  accomplished  by  an  opening  made  in 
direct  line  with  the  axis  of  the  pulp  canal.  In  general  terms  this 
involves  for  sound  teeth  an  opening  upon  the  lingual  surface  of 
incisors  and  cuspids  and  upon  the  occlusal  surface  of  bicuspids  and 
molars. 

This  access  may  consist  of  a  new  opening  or  an  extension  of  a 
cavity,  or  at  times  the  cavity  and  canal  may  simply  be  made  con- 
tinuous. 

When  a  cavity  of  decay  exists  the  pulpal  wall  should  be  perforated 
and  a  large  bud  bur  should  be  used  to  cut  away  the  dentin  over- 
hanging the  pulp  cavity.  It  is  usually  necessary  to  extend  the  cavity 
in  the  central  occlusal  direction,  so  as  to  permit  direct  access  to 
each  canal  (Figs.  455  to  462). 

When  a  tooth  crown  would  be  irremediably  weakened  by  such  a 

1  Dr.  J.  Foster  Flagg  had  such  a  case. 


THE  EXTIRPATION  OF  THE  PULP 


533 


course,  a  slight  indirectness  is  permissible  when  flexible  cleansers 
can  be  used  instead  of  drills.  This  leaving  of  tooth  structure  should 
be  done  with  judgment.  The  canals  must  be  cleansed.  In  cavity 
approaches  the  ouier  wall  of  the  pulp  cavity  should  be  cut  away  to 
permit  an  obtuse-angled  approach  rather  than  a  right-angled  one 
(Figs.  460  and  462,  A).  All  pulp  cavity  corners  should  be  burred  to 
a  shape  that  obviates  retention  of  pulp  debris,  the  subsequent  decom- 
position of  which  would  lead  to  discoloration.  The  opening  shown 
in  Fig.  458  is  faulty  for  this  reason,  and  is  better  if  extended  more 
toward  the  incisal  edge,  making  an  oblong  opening  with  rounded 
ends. 


Fig.  455 


Fig.  456 


Fig.  457 


Fig.  458 


I  B 


Fig.  459 


Fig.  460 


Fig.  461 


Fig.  462 


In  sound  teeth  the  entrance  to  the  canal  is  made  with  a  small 
spear  drill,  after  the  enamel  has  had  a  "spot"  made  in  its  surface 
with  a  sharp  dentate  bur.  This  centres  the  spear  drill  and  prevents 
its  slipping  about.  After  it  has  entered  the  pulp  cavity  dentate  burs 
are  used  to  enlarge  the  opening  to  the  desired  size  and  shape.  A 
sawing  motion  creates  more  rapid  clearance  and  cutting  of  tooth 
tissue. 

One  should  not  always  suppose  that  the  spear  drill  will  drop  into 
an  appreciable  pulp  cavity.     The  careless  driving  of  a  drill  into  a 


534     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

tooth  may  cause  a  perforation.  Secondary  dentin  or  a  large  nodule, 
and,  in  previously  treated  teeth,  zinc  phosphate  may  occupy  the 
pulp  chamber.  Therefore,  when  doubt  arises,  open  well  that  portion 
of  tooth  or  filling  which  has  been  drilled  through,  and  note  the 
conditions,  then  go  ahead  carefully.  In  opening  a  located  pulp 
chamber  with  burs  a  bud  bur  is  very  useful,  but  all  burs  once  placed 
through  the  drill  hole  and  into  the  pulp  chamber  must  be  used 
laterally  or  the  heel  of  the  bur  used  with  an  outward  sweep  toward 
the  occlusal  aspect  for  the  sake  of  safety. 

Fig.  463 


Kerr  or  Downie  broaches.    Various  finer  sizes  of  these  broaches  and  reamers  may 
be  had.    They  should  have  accurate  taper. 


The  canal  (or  canals)  is  now  to  be  explored,  and  if  of  operable 
size  a  Donaldson  cleanser  or  barbed  broach  is  passed  to  the  canal 
apex,  twisted  so  as  to  engage  its  teeth  with  the  pulp  substance, 
and  the  pulp  extirpated. 

If  there  be  any  difficulty  in  finding  the  canals  after  this  preparation, 
by  reason  of  the  broach  catching  on  the  edge  of  the  orifice,  the  mouth 
of  the  canal  should  be  made  continuous  with  the  wall  of  the  pulp 
chamber  by  means  of  a  small  bud  bur.  The  wall  then  leads  the 
broach  into  the  root  lumen. 

In  single-rooted  teeth  with  finer  apices  a  fine  Kerr  engine  root 
reamer  (Fig.  463)  may  be  passed  by  hand  to  the  apical  portion  of 
the  root  and  gently  rotated.  It  is  then  mounted  in  the  hand  piece, 
passed  gently  to  the  apex,  slightly  withdrawn,  and  then  operated  by 


THE  EXTIRPATION  OF  THE  PULP 


535 


engine  power.  It  is  pressed  lightly  laterally  to  enlarge  the  canal 
slightly.  The  next  larger  size  is  then  used  in  like  manner,  and 
finally  the  larger  admissible  sizes.  This  gives  a  beautifully  tapered 
canal  form  useful  in  canal  filling  and  for  the  adaptation  of  dowels. 
The  pulp  is  simultaneously  removed,  generally  being  churned  out 


Fig.  464 


Fig.  465 


Fig.  466 


Fig.  467 


Fig.  468 


Donaldson's  pulp-canal  cleansers. 


of  the  root,  and  danger  of  false  openings  is 
avoided.  A  final  exploration  and  apical 
scraping  may  be  given  with  a  fine  Don- 
aldson cleanser  (Figs.  464  to  466),  and 
the  pulp  cavity  corners  rounded  out  with 
burs. 

This  technique  is  only  admissible  in  cases 
of  openings  in  line  with  the  pulp  axis. 
Those  almost  in  such  line  may  have  the 
flexible  sizes  of  Kerr  reamers  so  used,  all 
apexward  pressing  and  reaming  to  be  done 
by  hand  at  first.  When  general  anesthesia 
is  employed  it  is  better  to  open  roughly, 
then  pass  a  fine  Donaldson  cleanser,  which 
has  been  previously  dipped  in  carbolic  acid 
and  laid  aside  in  readiness,  to  the  apex  of 
the  root  canal.  It  is  given  a  few  turns  to 
engage  the  pulp,  and  the  latter  is  lifted  away, 
to  be  done  upon  return  to  consciousness. 

As  the  Kerr  broaches  and  reamers  are  made  of  a  variety  of  forms, 
it  should  be  stated  that  only  those  w^hich  have  a  gradual  taper  from 
point  to  shank  can  be  relied  upon  to  satisfactorily  carry  out  this 


Donaldson's        spring-tem- 
pered nerve  bristles. 


The  other  work  is 


536      REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

technique.  In  these  the  successive  sizes  follow  one  another  without 
danger  of  perforation  of  the  canal  walls. 

It  is  sometimes  better  to  drive  a  fine  hand  Kerr  broach  to  the  canal 
apex,  and,  if  the  engine  broach  be  not  permissible,  to  continue  with 
the  different  sizes  of  hand  broaches.  One  soon  obtains  a  familiarity 
with  the  canal  curve  and  size  when  working  with  the  hand  which 
gives  confidence  and  safety  when  later  working  with  engine  power. 

In  molar  teeth  and  upper  first  bicuspids,  after  the  pulp  chamber 
has  been  prepared,  the  canals  are  to  be  located  with  a  fine  smooth 
broach  or  a  Kerr  broach.  The  finest  root  reamer  is  then  used  by 
hand  and  gently  twisted  and  forced  apexward  into  each  canal  in 
turn.  The  next  smaller  is  then  used.  As  these  canals  are  normally 
somewhat  curved,  only  flexible  forms  should  be  used  unless  the 
larger  size  follows  readily  the  rather  curved  canal  made  by  the 
previous  one.  Following  this,  Donaldson  cleansers  are  operated  by 
hand  to  scrape  the  sides  and  inequalities  of  the  somewhat  flattened 
canals  which  the  reamers  have  not  reached. 

In  place  of  drills  the  process  of  canal  enlargement  devised  by 
Callahan^  may  be  employed.  The  general  cavity  wall  is  varnished 
to  prevent  the  action  of  the  acid  upon  the  dentin,  and  by  means  of  a 
pair  of  Flagg's  dressing  pliers  or  a  minim  dropper  a  drop  of  sul- 
phuric acid  (50  per  cent,  solution)  is  deposited  at  the  mouth  of  the 
canal  to  be  operated  upon.  The  finest  size  of  Donalson's  canal 
cleanser  is  then  passed  into  the  canal  as  far  as  it  will  go,  using  a 
pumping  movement  to  carry  the  acid  farther  into  the  canal  and  to 
scrape  the  canal  walls  softened  by  the  action  of  the  acid.  The  acid 
chemically  destroys  any  organic  matter — i.  e.,  pulp  tissue — present, 
releases  the  calcium  of  the  dentin  from  its  combination,  and  forms 
calcium  sulphate,  which  is  mechanically  removed  by  scrapers.  Care 
must  be  observed  not  to  strain  the  broaches  too  greatly,  as  they  may 
break.  The  operation  is  continued  until  the  apex  of  the  root  is 
reached.  F.  T.  Hayes  suggests  the  use  of  aqua  regia  as  less  injurious 
to  broaches;  lactic  acid  is  also  less  injurious.  When  the  cleanser  will 
not  enter  readily  it  is  well  to  file  away  the  barbs  from  an  old  cleanser 
and  leave  it  roughened,  and  to  use  it  for  a  time  with  the  acid  until 
the  cleanser  proper  can  be  employed.  Even  then  it  may  be  necessary 
to  use  a  cleanser  with  only  part  of  the  barbs  filed  away.  Iridio- 
platinum  or  gold  broaches  may  be  used  for  this  purpose. 

Some  operators  prefer  the  use  of  the  alloy  kalium-natrium,  used 
on  the  broach  as  a  means  of  facilitating  the  opening  of  the  canals. 

In  the  canals  of  posterior  teeth  short  cleansers  are  mounted  in  a 

1  Proceedings  of  the  Ohio  State  Dental  Society,  1894. 


THE  EXTIRPATION  OF  THE  PULP 


537 


chuck  handle  and  the  shank  sharply  bent  at  a  right  or  obtuse  angle. 
If  the  cleanser  bind  in  the  canal,  it  should  be  grasped  with  the  thumb 
and  forefinger  and  given  a  straight  pull  to  relieve  it. 


Fig.  469 


Fig.  470 


Fig.  471 


Fig.  472 


If  acid  be  used  it  should  be  neutralized  with  sodium  bicarbonate 
or  sodium  dioxid.  The  improved  Gates-Glidden  drill  (Fig.  473) 
has  some  use  in  the  enlargement  of  canals  the  lumen  of  which  has 
been  determined  by  the  above  methods.  They  should  not  be  used 
for  the  preliminary  opening  of  fine  canals,  as  they  tend  to  form 
false  channels  in  the  side  of  the  canals  which  constantly  catch  even 
fine  bristles  and  may  render  a  canal  into  a  form  even  less  advan- 
tageous than  that  it  already  possesses.  The  canal  filament  of  pulps 
in  molars  and  upper  first  bicuspids  may  be  lifted  away  with  barbed 


538     REMOVAL  OF  DENTAL  PULP  AND  ROOT-CANAL  FILLING 

broaches  or  cleansers  if  the  canals  are  large,  but  it  is  ordinarily 
a  waste  of  time  to  attempt  it  in  the  finer  canals,  as  the  other  work 
must  be  done  in  the  apical  regions. 

The  use  of  5  per  cent,  formalin,  tannin,  or  alum,  to  be  specially 
applied  about  two  days  after  the  application  of  arsenic,  has  been 
suggested  for  the  toughening  of  pulps.  Their  use  necessitates  a  visit 
for  their  special  application.  They  toughen  the  pulp,  and,  while 
the  advantage  in  pulp  removal  is  offset  by  the  special  visit  needed, 
may,  in  fine  canals,  mummify  inaccessible  portions  of  pulp  tissue. 

The  point  of  importance  is  the  removal 
Fig.  473  from   the   pulp    canal    of   all  removable 

portions  of  pulp  tissue  and  an  enlarge- 
ment sufficient  to  admit  a  satisfactory 
root  filling.  It  is  an  open  question 
whether  in  multirooted  teeth  this  is  ever 
complete,  or  whether  it  is  necessary  that 
it   be   made   absolutely   so,  regardless  of 

Improved      Gates-Glidden  j.i         j  t  i  j  j.i, 

nerve-canal  drill  for  engine  o^hcr  dangers.  In  molars  and  even  other 
work.  teeth  there  may   be  more  than  one   for- 

amen and  at  times  delta-like  formations 
are  present.  Therefore  one  should  use  all  safe  means  and  rely  upon 
antiseptic  measures  for  the  impossible  cases.  In  this  connection  a 
radiograph  before  and  after  canal  exploration  will  be  of  assistance. 

A  perfectly  safe  rule  for  mechanical  procedures  is  as  follows:  Use 
drills  only  when  they  advance  readily  into  the  root  lumen;  prefer 
Downie  broaches  and  Donaldson  cleansers  under  other  circum- 
stances. Advance  no  large  reamers  into  delicate  apical  portions  of 
roots,  as  a  lateral  perforation  may  be  made.  If  a  fine  broach  cannot 
be  passed  through  the  apical  foramen,  do  not  attempt  its  enlarge- 
ment; and  it  is  better  to  preserve  a  normal  foramen,  as  large  for- 
amina present  greater  difficulty  of  filling  than  normal  ones. 

If  doubt  exist  as  to  the  presence  of  a  portion  of  pulp  in  the  apex 
of  the  root,  papain  paste  may  be  placed  in  the  canals  for  a  few  days 
to  digest  the  remaining  pulp  tissue.    (See  Pulp  Digestion.) 

If  the  pulp  be  removed  as  far  as  possible  by  careful  work  and  the 
canal  sealed  to  that  point  with  a  mechanically  perfect  and  anti- 
septic root  filling,  it  is  improbable  that  any  future  trouble  will  arise, 
and  it  is  better  that  any  such  trouble  should  be  subsequently  treated  than 
that  immediate  trouble  should  be  set  up  by  perforation  in  an  endeavor 
to  force  a  finding  of  canals  which  a  very  fine  Downie  or  Kerr  cleanser, 
or  broach,  will  not  explore. 

This  technique  is,  as  a  rule,  best  carried  out  under  rubber  dam,  to 
prevent  the  septic  contamination  of  canals  by  entrance  of  infected 


THE  EXTIRPATION  OF  THE  PULP  539 

saliva;  but  if  this  be  impossible  it  is  wise  to  sterilize  the  mouth  and 
napkin  it,  and  to  place  a  drop  of  carbolic  acid  or  formocresol  in  the 
canals  and  continue  the  work  under  antiseptic  precautions. 

It  is  wise  to  have  the  patient  first  brush  the  teeth,  using  soap  or  a 
tooth  paste  or  powder.  After  application  of  the  dam  or  napkin  the 
cavity  is  cleansed  of  the  debris  of  decay  if  any  be  present.  Then 
the  cavity  is  to  be  wiped  out  with  phenol  camphor.  Next  the  appli- 
cation of  cocain,  etc.,  is  made.  Before  entering  the  pulp  chamber 
or  just  after,  a  drop  of  formocresol  is  to  be  placed  on  the  field  of 
operation  and  a  clean  bur  used  to  enter  the  pulp  cavity.  The  debris 
is  removed,  the  canals  located,  and  a  fresh  drop  of  formocresol 
placed  before  continuing  with  the  canal  work. 

As  the  napkins  become  wet  they  may  be  removed,  the  cavity 
douched  with  a  jet  of  warm  water,  the  patient  rested  for  a  moment, 
and  then  the  napkins  are  reapplied,  the  cavity  dried,  and  the  opera- 
tion repeated.  The  napkins  may  be  renewed  without  disturbing  the 
treatment,  but  it  is  often  desirable  to  wash  out  the  debris,  and 
the  rest  is  often  agreeable  to  the  patient. 

The  scraping  of  the  canals  removes  the  possible  remnants  of 
pulp  tissue,  odontoblasts,  etc.,  adhering  to  the  dentin  walls,  and 
also  a  part  of  the  wall  with  the  large  ends  of  the  fibrils.  All  these 
are  decomposable  media,  may  become  septic,  and  are  wisely  removed. 

The  final  removal  of  all  pulp  debris,  coagulated  blood,  etc.,  is  best 
done  with  a  fine  Donaldson  cleanser,  moved  to  and  fro  in  the  canal 
with  one  hand,  while  with  the  other  a  stream  of  warm  water  is  gently 
introduced  by  means  of  a  Moffat  syringe.  A  large  cottonoid  roll 
or  a  napkin  may  be  held  by  the  patient  or  assistant  to  absorb  the 
excess  of  moisture  when  the  rubber  dam  is  in  position. 

If  the  operations  have  been  done  under  antiseptic  precautions, 
the  root  is  ready  for  filling,  unless  irritation  of  the  apical  tissues  be 
severe,  in  which  case  a  sedative  antiseptic— e.  g.,  menthol  in  chloro- 
form— on  cotton  should  be  sealed  in  the  canal.  The  gum  should  be 
painted  with  iodin  as  a  counterirritant,  and  the  subsidence  of  the 
symptoms  awaited.    (See  Non-septic  Apical  Pericementitis.) 

Rhein  recommends  for  the  treatment  of  inaccessible  portions  of 
recently  devitalized  pulps  the  use  of  a  chemically  pure  zinc  point, 
to  be  placed  in  the  root  moistened  with  a  1  to  500  mercuric  chlorid 
in  hydrogen  dioxid  (3  per  cent,  solution)  and  the  anode  of  the  cata- 
phoric appliance  applied  to  it,  the  cathode  sponge  to  be  placed  under 
the  dam  on  the  cheek.  From  1  to  5  milliamperes  of  current  are 
used  and  maintained  for  from  three  to  seven  minutes,  according  to 
the  exigency. 

Zinc  oxychlorid  is  produced  and  carried  into  the  tissue. 


540     REMOVAL  OF  DENTAL  PULP  AND    ROOT-CANAL   FILLING 

It  is  always,  perhaps,  safer  to  introduce  a  sealed  dressing  of  phenol 
camphor  plus  menthol  or  thymol  until  all  possible  hemorrhage  or 
irritation  has  subsided.  In  case  of  pressure  anesthesia  with  free 
hemorrhage  a  little  alum  and  thymol,  equal  parts,  is  well  added  to 
the  phenol  camphor,  or  even  a  dry  dressing,  to  absorb  any  secondary 
hemorrhage.     (Ottolengui.) 


DESCRIPTION  OF  FIGS.  474,  475,  AND  476.i 

Fig.  474. — Fig.  3  gives  in  contrast  a  sectional  view  of  deciduous  and  permanent  upper 
teeth  divided  through  their  lateral  diameters. 

Fig.  4,  a  sectional  view  of  the  corresponding  lower  teeth  divided  through  their 
anteroposterior  diameters:  a,  b,  c  represent  respectively  the  deciduous  and  permanent 
front  incisors  in  contrast;  d,  e,  f,  the  lateral  incisors;  g,  h,  i,  the  canines;  k,  deciduous 
molars,  upper  and  lower;  Z,  to,  the  successors  to  the  deciduous  molars,  the  bicuspids; 
n,  0,  represent  permanent  molars;  c,  /,  i,  m,  o,  have  dotted  lines  indicating  the  thickness 
of  enamel  removed  by  wear,  atrophy  of  the  cementum,  and  reduction  in  the  size  of  the 
pulp  due  to  progressive  calcification,  these  changes  being  incident  to  old  age. 

Fig.  475  erpresents  in  Fig.  1,  letters  a  to  h  and  a  to  h,  the  longitudinal  or  vertical 
sections  of  the  sixteen  upper  teeth,  showing  the  labiopalatal  diameter  of  the  pulp 
chamber  and  canal  in  crown  and  roots,  the  section  of  the  molars  being  through  the 
anterior  buccal  and  palatal  roots,  while  the  bicuspids  d  e  and  d£  illustrate  the  result 
of  such  a  compression  of  the  root  as  to  divide  the  pulp  chamber  into  two  canals — a 
condition  which  so  frequently  exists  in  these  flattened  roots.  The  double-lettered 
series,  d  d  to  h  h  and  dd  to  h_h,  represent  in  the  molars  a  section  through  the  posterior 
buccal  and  the  palatal  roots,  from  which  is  quite  readily  recognized  the  slightly  greater 
lateral  diameter  of  the  pulp  chamber  in  the  crown  and  the  larger  canal  in  the  posterior 
buccal  root  over  that  in  the  anterior  buccal  root,  while  the  bicuspids  lettered  e  e  d  d 
and  dd  e  e  illustrate  modified  pulp  chamber  and  canal,  with  bifurcation  of  the  root 
in  one,  these  being  cut  through  a  different  axis  or  plane  from  the  single-lettered  series. 

Fig.  2,  letters  a  to  h  and  a  to  ^  represent  the  sixteen  lower  teeth  with  the  section 
through  their  long  diameters,  as  in  the  upper  series.  These  incisors  illustrate  the 
compressed  or  flattened  condition  of  their  roots  in  contrast  with  the  cylindrical  char- 
acter of  the  roots  of  the  upper  incisors,  while  the  bicuspids  d  e  and  d_e  illustrate  the 
singleness  of  their  pulp  chamber  and  the  cylindrical  condition  of  their  roots  as  in 
contrast  with  the  flattened  or  compressed  condition  of  the  roots  of  the  upper  bicuspids. 
The  molars  /,  g,  h,  and  /,  g,  h  represent  sections  through  the  anterior  root,  illustrating 
its  compressed  condition  and  divided  pulp  chamber  in  the  first  and  second  molar, 
and  a  somewhat  flattened  one  in  the  anterior  root  of  the  third  molar;  ff,gg,  h  h  and 
f  f,  g  g,  hh  represent  the  single  and  cylindrical  pulp  chamber  in  the  posterior  root  of 
the  lower  molars,  while  hh,  cc  and  a  a,  hh  represent  the  incisors  and  canines  of  the 
same  series,  with  modifled  pulp  chambers  arising  from  modified  development. 

Fig.  476. — Fig.  1,  from  a  to  h  and  a  to  h,  represent  the  upper  teeth,  with  transverse 
or  horizontal  section  through  the  base  of  the  pulp  chamber  in  the  crown,  viewing 
the  entrance  to  the  canals  of  the  several  roots,  while  the  same  letters  in  Fig.  2  represent 
the  lower  series  in  the  same  manner. 

Fig.  3  represents  the  upper  teeth,  with  the  transverse  or  horizontal  section  made 
below  the  largest  diameter  of  the  pulp  chamber  and  through  the  canals  after  they 
have  diverged  from  the  central  chamber,  but  before  the  roots  into  which  they  run  have 
in  the  molars  bifurcated. 

Fig.  4  in  like  manner  represents  the  lower  series,  well  illustrating  the  flattened  or 
compressed  condition  of  the  canal  anterior  roots  of  the  molars  and  the  division  of  the 
chamber,  as  is  frequently  found  in  the  roots  of  the  lower  incisors. 

The  letters  a  a,hb,  c  c,  dd,  ff,  d  d,  and  e_e  (Fig.  3)  represent  the  relative  shapes, 
whether  circular,  oval,  or  flattened,  of  the  pulp  canal  in  the  roots  of  the  upper  central 
and  lateral  incisors,  the  canines,  the  flrst  and  second  bicuspids,  and  the  first,  second, 
and  third  molars,  while  the  same  letters  in  Fig.  4  represent  the  relative  shapes  of  the 
pulp  canal  in  simflar  teeth  in  the  lower  series. 

*  These  figures  are  taken  from  v.  Carabelli's  Anatomie  des  Mundes. 


SJc 


?:>'-> 


THE  EXTIRPATION  OF  THE  PULP 


543 


A. 


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«y  i^'^ 


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6) 


so 


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to 


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544     REMOVAL  OF  DENTAL  PULP   AND    ROOT-CANAL   FILLING 

Sometimes  it  is  desirable  to  mummify  any  possible  irremovable 
portion  of  pulp  or  the  fibrils  by  the  use  of  formalin  solutions  which 
are  usually  tolerated. 


Distal - 


Fig.  478        Fig.  479     Fig.  480 


mesial 


Diagram  illustrating  the  improvement  in  ac- 
cess C,  to  the  deeper  portions  of  enamel  by  cut- 
ting in  accordance  with  a  radiograph.  The 
dotted  line  shows  the  ordinary  opening  per- 
mitting the  access  b  b.    (Rhein.) 


Upper    lateral    incisors.    (Otto- 
lengui) . 


Fig.  481 


Fig.  482 


Fig.  484 


Upper  canines. 
Fig.  485 


Fig.  486 


Upper  first  bicuspids. 


The  carrying  out  of  canal  treatment  involves  a  knowledge  of  the 
topographical  anatomy  of  the  teeth  and  their  pulp  canals.  As  an 
aid  to  this  Figs.  474,  475,  and  476  are  introduced,  showing  the  normal 


THE  EXTIRPATION  OF  THE  PULP 


545 


outlines  of  the  teeth  and  their  pulp  chambers;  Fig.  476  shows  the 
appearance  and  locations  of  the  pulp  canal  openings  at  their  coronal 
ends.  It  is  to  be  borne  in  mind  that  the  roots  are  not  always  normal 
as  shown  in  Fig.  475,  and  that  various  degrees  of  lack  of  development 
or  resorption  may  cause  the  root  canals  to  be  unusually  open  or  short, 
with  the  treatment  complicated  by  the  presence  of  vital  tissue  at  the 
root  ends.  In  a  general  way  it  may  be  stated  that  much  resorbed 
roots,  as  indicated  by  the  age  in  deciduous  teeth,  or  largely  incom- 
plete roots,  as  indicated  by  the  age  in  permanent  teeth,  indicate 
a  pulp-capping  operation  rather  than  extirpation;  in  the  permanent 
teeth,  to  permit  better  root  formation.  If  unavoidable,  one  must 
do  the  best  possible. 


Fig.  487 


Fig.  488 


Upper  second  bicuspid. 
Fig.  489  Fig.  490 


Upper  first  molar. 

Fig.  491 


V'  i 


Upper  molar. 


Upper  second  molars. 


In  the  penetration  and  enlargement  of  canals  the  larger  and 
straighter  canals  may  be  cleansed  thoroughly  to  the  apex,  but  in 
very  fine  and  tortuous  roots  (Figs.  478  to  507)  the  operator  is  often 
confronted  with  the  option  of  taking  the  chances  of  perforation 
by  forcing  further  entrance  or  of  leaving  some  doubtful  apical 
portion  uncleansed.  To  further  perfect  the  operation  of  canal  cleans- 
ing a  radiograph  may  be  taken  as  indicated  by  Rhein,  and  the 
cavity  extension  made  so  as  to  permit  as  direct  an  access  as  possible 
(Fig.  477).  In  very  bad  cases  the  decision  should  be  that  the  danger 
35 


546      REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

of  perforation  is  the  greater  evil,  and  agents  of  a  mummifying 
character  should  be  employed  to  render  any  such  filament  into  a 
state  lessening  the  danger  of  subsequent  putrefaction. 


Fig.  492 


Fig.  493 


Fig.  494 


Fig.  496 


Fig.  497 


Upper  molars.  (Ottolengui.) 
Fig.  498  Fig.  499 


Q 


Upper  third  molars. 

The  writer  regards  the  use  of  formocresol  (equal  parts  of  37  per 
cent,  aqueous  formaldehyd  solution  and  cresol)  as  especially  valu- 
able where  immediate  root  filling  is  not  indicated.  If  the  patient  be 
of  a  nervous  and  irritable  type  this  may  be  diluted  to  5  or  10  per  cent, 
formaldehyd  strength  by  the  use  of  cresol  or  camphophenique  with- 
out impairing  its  value.  Often  the  full  strength  may  be  used  on 
cotton  as  a  temporary  dressing.  This  hardens  any  remaining  pulp 
and  also  probably  the  fibrils  in  the  tubules.  It  also  permits  the 
apical  tissue  to  heal  and  resume  its  normal  sensitivity  when  the 
pulp  has  been  entirely  removed,  which  is  of  value  in  determining 
the  extent  to  which  pressure  may  be  applied  in  filling  the  canals. 
In  anterior  teeth  it  is  better  to  use  aqueous  formaldehyd  solutions, 
as  the  cresol  may  cause  discoloration,  but  in  these  situations  more 
perfect  mechanical  work  can  be  done. 


THE  EXTIRPATION  OF  THE  PULP 


547 


In  a  few  cases  in  which  cervical  cavities  obHterate  the  canal  or 
cause  annoying  approach  to  it,  it  is  desirable  to  remedy  the  con- 


FiG.  500 


Fig.  504 


Fig.  501 


Lower  bicuspids. 
Fig.  503 


Lower  first  molars. 


Fig.  502 


Fig.  505 


Lower  first  molar. 

Fig.  506 


Lower  second  molar. 


Lower  first  molar,  immature. 
Fig.  507 


Lower  third  molar. 


dition.  In  such  case  the  canals  are  opened  as  usual  and  enlarged, 
and  the  cavity  prepared  with  suitable  retentions  for  filling.  The 
last-used  reamer  is  then  to  be  placed  in  the  canal  and  the  filling 


548     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

inserted.  The  filling  is  then  supported  by  pressure  while  the  reamer 
is  slowly  twisted  to  the  right  and  withdrawn,  leaving  a  canal  through 
the  filling.    This  may  be  done  with  amalgam  or  with  zinc  phosphate 

if   a   later   removal  be  required.     If   the 
Fig.  508  root  be  much  weakened,  a  tapering  dowel 

may  be  cemented  through  the  crown 
and  canal,  thus  attaching  the  root  to  the 
crown  more  firmly  (Fig.  508,  also  p.  432). 

ACCIDENTS   IN   CANAL    OPENING. 

The  chief  accidents  that  may  occur  are 
the  perforation  of  the  root  wall  and  the 
breaking  of  the  instruments  used.    If  the 
technique  laid  down  be  carefully  followed 
Method  of   restoring  lost     the   danger  of    perforation    is   practically 

canal  continuity.     The  cavity         t*j.i        tpj.j.1  j.j.i 

should  have  more  retention  elimmated.  In  fact,  the  greatest  danger 
form  than  shown:  a,  amalgam,      is  the  penetration  and  enlargement  of  the 

apical  foramen.  To  avoid  this  the  Kerr 
reamers  should  always  be  passed  to  the  apex  of  the  canal  by  hand 
or  while  the  reamer  is  not  revolving.  It  is  then  withdrawn  a  trifle  and 
revolved,  and  one  may  always  judge  the  distance  the  reamer  was 
withdrawn.  Accidents  are  usually  the  result  of  thoughtless  forward 
pressure  of  reamers  and  drills,  and  care  will  reduce  this  to  a  minimum. 
Sometimes  one  must  take  the  chances  with  the  Kerr  engine  reamer. 
When  doubt  exists  as  to  canal  locations,  the  desiccation  of  the 
pulp  chamber  is  of  great  assistance  by  bringing  them  into  view,  and 
if  secondary  deposits  exist  one  should  always  use  a  small  bud  bur 
and  keep  well  within  the  limits  of  the  dentin  of  a  root  while  gently 
seeking  a  canal  lumen. 

Frequent  exploration  should  follow  gentle  advances,  and,  as  a 
rule,  the  canal  will  be  found  of  fairly  normal  size  just  beyond  the 
point  of  constriction.  In  some  cases  50  per  cent,  sulphuric  acid 
should  be  sealed  against  the  suspected  canal  and  the  operation 
deferred  to  another  sitting. 

If  a  perforation  be  accidentally  made  it  should  be  covered  as  in 
any  case  of  perforation  (which  see). 

Always  one  should  be  able  to  diagnosticate  such  an  opening  and 
arsenic  should  never  be  applied  to  such.  Cases  of  extensive  necrosis 
have  occurred  from  carelessness  in  this  direction.  The  breakage  of 
broaches  is  largely  avoidable  through  the  use  of  new  instruments  and 
by  adhering  to  the  rule  of  using  the  smaller  sizes  until  the  canals  are 
sufficiently  enlarged  to  permit  the  use  of  larger  sizes,  and,  in  case  of 


ACCIDENTS  IN  CANAL  OPENING 


549 


Fig.  509 


engine  reamers,  of  starting  the  power  with  the  reamer  loose  in  the 
canaL  The  engine  broach  seems  to  be  of  better  temper  than  the 
engine  reamer. 

Accidents  of  this  sort  usually  occur  with  barbed  instruments  of 
the  Donaldson  cleanser  type,  especially  when  used  with  force. 
Sulphuric  acid  tends  to  disintegrate  the 
broach,  so  that  lactic  acid  is  often  better 
used  with  it,  or  the  alloy  of  sodium  and 
potassium  with  a  smooth  broach  will  open 
the  canal  so  that  the  cleanser  will  not  bind. 
If  it  does  it  should  be  grasped  with  the 
thumb  and  finger  and  given  a  straight  pull. 

While  avoidance  is  far  better  than  the  ap- 
plication of  the  remedy,  if  the  accident  occur, 
the  broach  sh6uld  be  removed  if  possible. 

If  lying  loosely  in  the  canal  a  new  cleanser 
may  be  passed  to  one  side  of  it  and  then  be 
pressed  against  it.  It  should  engage  the 
barbs  and  jig  it  cut. 

Cotton  wrapped  on  a  small  Swiss  broach 
may  be  pressed  down  at  one  side  of  the 
broken  broach  and  its  fibres  made  to  engage 
its  barbs. 

Moving  the  broach  back  and  forth  while 
sulphuric  acid,  sodium  dioxid,  or  sodium  and 
potassium  is  about  it,  will  sometimes  loosen 
it.  One  may  sometimes  drill  to  one  side  of  a 
broken  instrument  with  a  Kerr  hand  broach 
in  order  to  more  readily  engage  it  with  a 
barbed  instrument.  If  very  loose  a  magne- 
tized probe  will  attract  it  and  draw  it  out. 

If  the  broach  be  tightly  fixed  in  the  canal, 
sodium  chlorid,  tincture  of  iodin,  sulphuric 
acid,  aqua  regia,  or  25  per  cent,  pyrozone 
may  be  sealed  in,  in  the  hope  of  chemically 
disintegrating  it. 

The  head  of  a  Gates-Glidden  drill  or  Kerr 
reamer  is  treated  in  the  same  manner.  Some- 
times in  straight  roots  the  How  appliance  shown  in  Fig.  509  is  useful 
If  any  broach  be  irremovable,  iodoform  paste  or  embalming  paste 
should  be  packed  over  it  and  sealed  in,  in  order  to  keep  the  part 
permanently  sterile.  In  a  septic  case  the  formocresol  treatment 
should  precede  such  root  filling. 


Split  and  threaded  in- 
strument for  engaging 
the  shank  of  a  Gates- 
Glidden  drill. 


550     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

THE    FILLING    OF   ROOT    CANALS. 

In  all  cases  in  which  the  removal  of  the  dental  pulp  from  the 
canals  is  necessary,  it  is  imperative  that  the  pulp  canals  shall  be 
filled  with  some  substance  that  shall  mechanically  obliterate  it 
by  sealing  it  throughout  its  length,  in  order  to  prevent  the  ingress 
of  fluid  either  from  the  mouth  or  apical  tissue.  Such  fluid  is  liable 
to  putrefaction,  and  the  results  of  putrefaction  follow.  If  made 
antiseptic,  it  also  tends  to  kill  out  any  bacteria  which  may  find 
a  partial  entrance.  The  mechanical  sealing  may  be  defective,  even 
when  the  best  possible  effort  is  put  forth  to  make  it  perfect,  so  that 
the  addition  of  more  or  less  permanent  antiseptics  is  valuable. 
Prinz  has  suggested  that  it  should  be  impervious  to  a:-rays  so  that 
it  may  be  radiographed. 

It  matters  little  whether  a  canal  filling  is  hard  or  soft  provided  it 
seals  the  canal  permanently,  that  it  is  permanently  antiseptic,  non- 
irritating,  and  that  it  is  not  disturbed  by  any  subsequent  work.  It 
is  better  that  it  be  capable  of  removal  with  a  reasonable  amount  of 
safe  work. 

It  also  makes  very  little  difference  whether  the  pulp  has  been 
removed  while  aseptic  or  has  been  in  a  septic  state,  provided  the 
canal  has  been  rendered  sterile  by  appropriate  means. 

In  other  words,  when  the  canal  is  aseptic  and  the  apical  tissues 
sterile  and  healthy,  the  canal  is  ready  for  filling.  The  length  of  time 
this  may  require  also  makes  no  difference.  Therefore,  what  is  here 
said  applies  to  all  cases  requiring  root  filling.  Much  has  been  written 
of  the  impossibility  of  sterilizing  the  tubules  of  root  canals  and  of 
the  liability  of  return  of  sepsis  from  bacteria  located  in  them.  This 
simply  means  that  one  should  employ  the  best  means  of  gaining 
sterility  known  and  then  employ  permanent  antiseptics.  To  seal 
and  keep  these  tubules  as  sterile  as  possible,  the  use  of  a  thin  varnish 
of  resin,  12  grs.,  in  chloroform,  fSiijj  has  been  suggested  by  Callahan 
to  be  applied  after  desiccation  and  before  root  filling.  The  size  of 
the  apical  foramen,  the  presence  of  inaccessible  apical  portions  of 
canals,  the  presence  of  perforations  and  some  other  conditions, 
however,  indicate  a  choice  of  some  root  filling  rather  than  others, 
so  that  there  is  no  absolute  rule  for  all  cases. 

The  following  root  canal  fillings  are  useful. 

Gutta-percha. — This  is  usually  the  ordinary,  low  heat,  pink  gutta- 
percha base  plate  containing  vermilion  and  zinc  oxid.  Cones  may 
be  rolled  or  left  with  fiat  sides.  Prepared  cones  may  be  purchased 
which  have  an  accurate  taper  and  are  either  round  or  flat-sided. 
The  flat  side  permits  any  adjunct  plastic  filling  material  or  solvent 


THE  FILLING  OF  ROOT  CANALS  551 

to  flow  down  the  side  of  the  cone  rather  than  be  forced  tow^ard  the 
apex. 

Temporary  stopping  may  be  melted  in  a  spoon  and  aristol  added 
to  it.  It  is  then  rolled  into  cones  for  use.  Instead,  a  stick  of  it  may 
be  warmed  at  a  point  away  from  the  end  and  then  be  pulled  out  into 
two  cones  which  may  be  further  rolled  out.  They  may  be  rolled  in 
powdered  aristol  if  desired. 

Ottolengui  advises  the  use  of  bits  of  floss  silk  an  inch  long  to  be 
saturated  with  chloro-percha  and  dried.  These  are  to  be  pressed 
into  chloro-percha  previously  placed  in  the  canal  and  crimped  to 
place.  An  end  is  left  projecting  into  the  pulp  chamber.  If  necessary 
this  may  be  caught  and  the  dressing  withdrawn. 

Chloro-percha. — This  is  a  solution  of  gutta-percha  base-plate  in 
chloroform.  Usually  a  quantity  of  aristol  or  iodoform  is  added  to 
make  it  antiseptic.  As  it  shrinks  in  hardening  it  should  be  used  in 
conjunction  with  gutta-percha  cones  or  carried  upon  cotton  twist 
or  upon  floss  silk,  which  it  saturates,  transforming  them  practically 
into  a  solid  mass  when  the  chloroform  evaporates. 

Euca-percha. — The  basis  of  this  substance  is  a  solution  of  gutta- 
percha base-plate  in  eucalyptol.  To  this  various  antiseptics  may 
be  added.  There  are  various  modes  of  making  this  substance. 
B.  L.  Cochran^  suggests  the  following: 

I^ — Gutta-percha  base-plate oss 

Dissolve  in  chloroform  q.  s.  to  a  thin  solution.  ^ftil*!^ 

Add  saturated  solution  of  thymol  in  eucalyptol    .       .       .  fgss 

Let  the  chloroform  evaporate. 

Euca-percha  Compound  (Buckley,  Lilly)  is  a  simple  solution  of 
base-plate  in  eucalyptol  made  by  aid  of  heat. 
'   Formo-percha  (Blair)  has  paraform  and  oil  of  cassia  added. 

This  material  may  be  warmed  into  a  creamy  paste  and  be  used 
either  on  cotton  or  be  used  in  conjunction  with  gutta-percha 
cones. 

Zinc  Oxychlorid. — This  consists  of  the  ordinary  zinc  oxychlorid 
cement,  wdiich  consists  of  modifled  calcined  zinc  oxid  for  the  powder 
and  diluted  zinc  chlorid  as  the  fluid. 

It  is  antiseptic  for  a  time  at  least,  and  may  have  iodoform  incor- 
porated with  it  if  desired.  It  is  carried  to  place  on  a  thread  of  cotton, 
or  may  be  used  with  gutta-percha  cones.  The  addition  of  a  trifle 
of  glycerin  retards  setting. 

Embalming  Paste. — A  so-called  embalming  paste  is  prepared  as 
follows : 

Dental  Review,  1905. 


552     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 


Or, 


I^ — Paraform 1  part 

Thymol       .      .    * 1  part 

Glycerin 1  part 

Zinc  oxid 1  part  or  more. 

I^ — Paraform 1  Part 

Thymol       .       .      '. 2  parts 

Alum 1  part 

Zinc  oxid 2  parts 

Creosote  to  a  thick  or  thin  paste. 


This  is  used  as  a  temporary  germicidal  canal  dressing  on  cotton 
or  as  a  root-filling  with  gutta-percha  or  temporary  stopping  cones 
which  are  pressed  into  it. 


Fig.  510 


Fig.  511 


Radiograph  of  a  perfect  gutta-percha  root 
filling.   (Rhein.) 


Root-canal  filling:  A,  gutta-percha; 
B,  zinc  oxychlorid. 


Wax  or  Paraffin. — Either  of  these  may  have  a  third  of  its  bulk  of 
salol,  aristol,  or  iodoform,  or  a  fifth  of  paraform  added  to  it  while 
melted  in  a  spoon.  It  is  then  rolled  into  cones  or  small  pellets.  In 
use  a  pellet  is  dropped  into  the  dried  pulp  chamber  and  a  hot  Evans 
root  drier  point  applied.  As  it  melts,  the  metal  point  is  carried  down 
into  the  root  and  the  fluid  material  pumped  to  the  apex.  Capillarity 
does  part  of  the  work.  It  adjusts  itself  to  the  tissue  and  the  canal 
walls.  The  pulp  chamber  is  then  cleared  of  excess  wax,  etc.,  and 
filled  without  pressure. 

Prinz^  recommends  the  use  of  hard  paraffin  having  a  melting 
point  of  not  less  than  132°  F.  in  the  following  combination: 

R — Thymol •  .       .       .      .        2  parts 

Bismuth  trioxid 30  parts 

Hard  paraffin 68  parts 

The  canal  is  to  be  thoroughly  dried,  then  merely  moistened  with 
liquid  albolenCj  a  cone  of  the  compound  then  to  be  placed  in  the 


1  Dental  Cosmos,  October,  1912,  p.  1089. 


THE  FILLING  OF  ROOT  CANALS 


553 


canal  and  melted  with  a  root  drier  (an  electric  drier  or  Evans'  or 
Reithmiiller's  modification^).  The  albolene  combines  with  it  and 
leads  it  to  place  with  exclusion  of  air.  The  bismuth  is  added  to 
make  it  impervious  to  the  .r-rays,  hence  it  throws  a  radiographic 
shadow. 

Prinz  states  that  iodoform  added  to  paraffin  can  be  only  super- 
ficially antiseptic.  This  is,  however,  quite  sufiicient.  IMixed  into 
wax  it  persistently  odorizes  the  air  in  its  vicinity,  hence  should 
have  antiseptic  value.  The  influence  of  iodiform  for  long  continued 
usefulness  is  unquestionable. 

Salol. — This  is  a  solid  antiseptic,  melting  at  104°  F.  It  is  used 
much  as  paraffin  is.  A  gutta-percha  cone  may  be  thrust  into  it 
while  fluid.  It  often  seems  to  disappear  from  canals,  and  unless 
used  with  paraffin  is  to  be  used  only  as  a  temporary  root  filling. 


Fig.  512 


Fig.  513 


A,  perforation  through  side  of  apex; 
D,  cone  of  gutta-percha  passing  through ; 
B,  portion  to  be  cut  off;  C,  portion  of 
canal  not  treated. 


Lateral  perforation  due  to  holding  a 
bur  at  a  wrong  angle  to  the  axis  of  the 
root:  A,  root  canal  subsequently  filled 
with  gutta-percha;  5,  perforation  filled 
with  a  fitted  cone  of  gutta-percha;  C, 
zinc  oxy-chlorid. 


Canada  Balsam. — A  solution  of  Canada  balsam  in  chloroform  to 
which  hydronaphthol  is  added  (Williams)  makes  a  useful  solution 
in  which  to  saturate  cotton  twists  or  to  moisten  canals  previous  to 
the  introduction  of  a  cone  of  gutta-percha.  Balsam  of  Peru  is  now 
on  trial,  but  its  soft  condition  is  liable  to  render  it  a  failure. 

Colophony. — Callahan^  recommends  violin  resin,  grain  12,  in  chloro- 
form, 3  fiuidrams,  as  a  thin  solution  for  filling  the  desiccated  tubuli. 
The  canals  having  been  reamed  to  permit  cones  to  enter,  they  are 
filled  w^ith  the  solution  and  a  gutta-percha  cone  pumped  back  and 
forth  forty  to  sixty  times  to  dissolve  the  cone  and  force  adaptation. 
The  cone  is  then  packed  in  with  pluggers  touched  to  a  cake  of 
paraffin. 

1  See  Dental  Cosmos,  March,  1913,  p.  342. 
^  Journal  of  the  Allied  Sciences,  March,  1914. 


554     REMOVAL  OF  DENTAL  PULP  AND    ROOT-CANAL   FILLING 

Normal  Tapering  Well-opened  Canals. — In  these  canals  gutta-percha 
is  admirable;  a  little  eucalyptol  is  applied  to  the  canal  walls  and  a 
section  of  a  suitable  cone  mounted  by  heat  on  the  end  of  a  canal 
plugger  which  will  go  to  or  nearly  to  the  canal  end  is  gently  but 
firmly  pressed  into  the  apex  of  the  canal.  Temporary  stopping  cones 
are  more  readily  adapted,  and  as  they  can  be  made  antiseptic,  are 
valuable. 

The  rest  of  the  canal  is  then  filled  with  other  sections  or  with  zinc 
oxychlorid  made  thin  and  carried  to  place  on  cotton  twists.  The 
latter  may  be  used  for  the  entire  canal,  and  should  then  be  preceded 
by  a  tiny  bit  of  cotton  saturated  with  an  essential  oil  to  prevent 
irritation  of  the  apical  tissue.  It  is  claimed  that  this  cotton  is  acted 
upon  by  the  zinc  chlorid,  being  transformed  into  an  amyloid  condition. 
If  used  alone  a  slight  degree  of  moisture  aids  in  carrying  to  the 
apical  foramen  (Fig.  513). 

A  variant  consists  in  moistening  the  canal  with  chloro-percha  or 
euca-percha,  and  using  the  section  of  cone  or  pressing  in  an  entire 
cone.  A  second  cone  may  be  placed  at  the  side  of  the  first  and 
both  compacted  after  warming  with  a  hot  air  blast,  or  the  first  cone 
alone  used. 

Another  variant  is  the  use  of  chloro-percha  on  cotton,  which  makes 
a  very  accurate  and  easily  introduced  root  filling  when  carried  to 
place  on  a  properly  formed  and  tempered  Swiss  broach  or  prepared 
Donaldson  bristle.    A  little  iodoform  may  be  taken  up  with  it. 

When  the  broach  must  be  bent  to  enter  canals,  loosen  the  broach 
first  before  introducing  into  the  canal,  thus  leaving  the  cotton 
loosely  mounted  on  the  broach.  To  prepare  a  Donaldson  bristle  cut 
off  the  hook  and  flatten  the  end  upon  an  Arkansas  stone,  and  slightly 
flatten  on  two  sides,  then  lay  upon  a  glass  slab  and  burnish  thor- 
oughly to  remove  any  bur  left.  In  use  the  cotton  and  broach  are 
rolled  with  the  left  forefinger  and  thumb  only.  It  is  obvious  that 
to  do  this  the  .broach  must  be  perfectly  straight.  When  slightly 
bent  the  method  of  rolling  the  cotton  next  described  may  be  em- 
ployed. The  writer  believes  the  prepared  Swiss  broach  not  only 
more  facile  but  economical  in  use. 

To  prepare  broaches,  select  accurately  tapering  Swiss  or  English 
broaches  from  which  the  temper  has  not  been  drawn.  Next,  draw 
the  temper  by  placing  a  few  in  a  test-tube  and  heating  first  at  the 
shank,  graduahy  drawing  the  tube  over  the  flame  toward  the  points. 
The  blue  color  seen  on  the  shank  should  be  run  out  to  the  tip;  let 
cool  on  any  open  surface.  The  soft  broaches  usually  sold  are  nearly 
useless.  The  point  is  left  if  canal  exploration  is  intended.  For 
carrying  cotton  twists,  cut  the  end  off  with  scissors.    To  wind  the 


THE  FILLING  OF  ROOT  CANALS 


555 


cotton  lay  a  wisp  on  the  left  forefinger,  lay  the  broach  upon  it,  close 
down  the  thumb,  then  quickly  revolve  the  broach  with  the  right 
forefinger  and  thumb,  pushing  the  cotton  through  those  of  the  left 
hand  to  form  a  symmetrical  cone.  To  use  as  a  swab,  rotate  in  the 
canal  to  the  right.  To  leave  the  cotton  in  the  canal,  rotate  to  the 
right  as  the  twist  is  pressed  to  the  apex.  Then  turn  the  broach  once 
or  twice  to  the  left  to  loosen  it  from  the  cotton,  withdraw  a  little, 
then  press  in  again.    Thus  the  cotton  is  crimped  upon  itself. 

Roots  with  Open  Foramina.^ — These  may  be  incomplete  roots  with 
very  large  apical  openings,  in  which  case  wax  with  aristol  is  the  best 
filling  used,  as  previously  stated.  It  should  be  said  again,  however, 
that  if  possible  the  pulp  of  such  a  tooth  should  be  capped  to  permit 
root  formation  to  be  completed. 

Fig.  515 


Manner  of  measuring  the  length  of  a  root 
and  fitting  a  gutta-percha  cone. 


-a 


Manner  of  tapering  a  canal  to  fit  a 
cone  of  the  same  size. 


If  the  foramen  is  of  moderate  extent  and  either  natural  or  unfor- 
tunately made  with  drills,  gutta-percha  cones  are  valuable.  To 
determine  the  size  of  the  cone,  one  of  two  methods  may  be  employed. 
Perhaps  the  more  accurate  is  the  employment  of  a  series  of  gradually 
increasing  sizes  of  canal  pluggers.  One  should  be  selected  which  will 
just  fit  the  apex  or  be  a  trifle  too  large.  By  placing  this  in  the  hole  of 
a  draw  plate,  a  specially  rolled  cone  or  even  a  slightly  tapering  size 
may  be  made  to  fit  the  hole  in  the  plate.  The  canal  is  moistened  with 
eucalyptol  or  chloro-percha  and  a  quarter-inch  section  of  the  cone  is 
carried  on  the  plugger  to  its  place  in  the  root-canal  apex.  A  slight 
protrusion  is  not  ordinarily  productive  of  injury.  A  cardboard  per- 
forated by  the  respective  plugger  will  do  instead  of  the  draw  plate. 
If  the  root  length  was  previously  measured  with  a  piece  of  rubber 
dam  slipped  over  the  plugger  shank  and  some  know^n  point  on  the 


556     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL  FILLING 

tooth  used  as  a  guide,  the  cone  should  be  seen  to  go  down  until  it 
chokes  the  foramen,  when  the  dam  should  be  above  the  guide  point 
a  distance  equal  to  the  length  of  the  cone  section  used. 

In  the  second  method  a  long,  tapering  cone  is  prepared.  Some 
point  on  this  must  fit  the  foramen.  It  is  tried  in  and  as  often  as 
sensation  is  felt  it  is  cut  off  a  trifle  and  tried  again  until  it  chokes 
the  foramen  without  sensation. 

In  case  of  abscess,  especially  if  filling  is  a  means  to  a  cure,  this 
may  extend  beyond  the  apex  of  the  tooth. 

The  cone  should  be  marked  at  a  point  corresponding  to  the  guide 
point  chosen  and  be  laid  aside.  Next,  a  fine  hook  made  by  bending 
the  tip  of  a  fine  broach  to  a  right  angle,  then  cutting  it  close  to  the 
shank,  has  a  piece  of  rubber  dam  slipped  over  it  and  is  passed  through 
the  apex  and  hooked  upon  the  edge  (Fig.  514).  The  dam  is  slipped 
to  the  chosen  guide  point.  The  probe  hook  is  withdrawn,  the  dam 
laid  at  the  mark  on  the  cone,  and  the  cone  cut  off  at  the  lower  edge 
of  the  hook  (Fig.  514,  b).  In  use,  a  little  solvent,  preferably  chloro- 
percha,  is  placed  in  the  canal  and  the  cone  slowly  slipped  to  place 
until  the  mark  coincides  with  the  guide  point.  The  cone  is  then  cut 
off  with  a  hot  instrument,  warmed,  and  gently  packed  into  the  canal. 

When  the  canal  has  been  reamed  with  a  small  engine  reamer,  and 
the  apex  enlarged,  the  hook  may  be  placed  and  have  a  bit  of  rubber 
dam  on  it  as  a  guide.  Then  slip  a  bit  of  dam  over  a  larger  tapering 
root  reamer  at  a  corresponding  length.  Drive  the  reamer  in  until  at 
the  guide  point.  This  gives  a  tapering  cone  shape  to  the  canal  and 
is  a  guide  in  the  construction  of  the  cone  (Fig.  515). 

In  some  cases  of  large  foramina  or  perforation  a  bit  of  sterile 
grafting  sponge  may  be  introduced  into  the  apical  space  and  the 
filling  placed  against  it.^ 

Canals  with  Inaccessible  Apices. — Any  tissue  in  such  apices  should 
have  been  mummified  or  sterilized  with  formocresol  or  be  treated 
by  Rhein's  method^  of  filling  a  canal  with  mercuric  chlorid  in  hydro- 
gen dioxid  (1  to  500),  passing  in  a  zinc  probe,  then  applying  the 
anode  of  a  cataphoric  outfit  with  from  1  to  5  milliamperes  of  current 
from  three  to  seven  minutes  (the  cathode  at  the  cheek).  The  object 
is  to  form  zinc  oxychlorid  in  the  apical  root  canal  through  electro- 
lytic action.  The  canal  must  be  regarded  as  doubtful,  but  if  well 
opened  to  the  inaccessible  portion  a  trifle  of  formo-percha  may  be 
placed  on  cotton  at  this  point  and  the  balance  of  the  canal  be  filled 
with  antiseptic  temporary  stopping.  The  paraform  and  cassia  in  the 
formo-percha  are  active  agents. 

1  G.  Brunton,  England:  Dental  Cosmos,  1900. 
z  Dental  Cosmos,  1905,  p.  1196. 


THE  FILLING  OF  ROOT  CANALS  557 

A  variant  consists  in  the  use  of  embalming  paste  or  Soderberg's 
mummifying  paste,  either  made  stiff  and  introduced  with  successive 
sizes  of  phiggers,  beginning  with  the  largest  admissible  and  proceeding 
to  the  smallest,  or  moistening  the  canal  with  the  thinner  paste  and 
packing  a  cone  into  it.  The  use  of  such  a  paste  in  connection  with  a 
cone  of  gutta-percha  is  valuable  as  an  agent  embalming  the  fibrils 
in  the  dentin  of  teeth  from  which  living  pulps  have  been  removed, 
or  of  keeping  sterile  the  tubules  of  those  teeth  in  which  the  pulp 
is  gangrenous  (see  p.  559) . 

If  conditions  admit  of  it,  provision  for  future  entrance  of  the  canals 
should  be  made,  and  it  is  always  well  to  divide  the  operation  of 
canal  filling  and  crown  filling  by  a  short  period  of  time. 

Iodoform  paste  with  or  without  cotton  may  be  placed  in  the  apical 
third  of  the  canal. 

Root  Canals  in  Temporary  Teeth. — These  may  at  times  be  well  filled 
with  gutta-percha  points,  which,  if  aseptic,  do  not  interfere  with 
resorption,  but  a  material  of  easier  adaptation  which  absorbs  with 
the  root  is  preferable.  The  waxes  meet  the  indications,  as  they  can 
be  pumped  while  fluid  from  the  action  of  a  hot  root  drier  into  all 
inequalities,  where  they  adjust  their  relation  to  the  soft  tissue. 

Buckley  recommends  in  cases  of  chronic  abscess  the  use  of  a  stiff 
mixture  of  calcium  phosphate  and  formocresol  (formalin,  1  part; 
cresol,  2  parts),  to  be  packed  into  the  pulp  cavity  and  zinc  phosphate 
flowed  over  it. 

Johnson  recommends  euca-percha  to  be  pumped  into  the  canals 
and  pressure  with  temporary  stopping  to  be  exerted  until  the  solution 
appears  at  the  fistula.  Such  temporary  stopping  as  does  not  interfere 
with  filling  integrity  should  be  left. 

There  are  various  other  methods  of  filling  root  canals,  such  as 
driving  wood  points  saturated  in  carbolic  acid  into  the  canals;  the 
use  of  iodoform  paste,  with  or  without  cotton,  or  of  creosote  on  cotton 
(preferably  raw  cotton);  the  use  of  balsamo  del  deserto,  etc.,  which 
have  had  advocates,  but  the  methods  given  are  those  which  have 
had  long-continued  and  successful  use. 

The  Covering  of  the  Root  Canal  Filling. — The  bulb  of  the  pulp 
chamber  may  be  filled  with  any  of  the  more  solid  materials.  In  case 
of  a  strong  crown,  temporary  stopping  makes  a  good  occupant  of 
this  cavity,  though  gutta-percha  is  often  used;  oxychlorid  of  zinc 
aids  in  keeping  good  color.  In  the  weaker  teeth  or  sometimes  for 
other  reasons  the  final  filling  may  extend  into  the  pulp  canal  to 
assist  in  anchorage. 

Partial  Removal  of  Pulp.^ — The  Cobalt  method  of  pulp  treatment 
has  been  alluded  to.    Wm.  Herbst,  of  Bremen,  advanced  the  idea 


558     REMOVAL  OF  DENTAL  PULP  AND   ROOT-CANAL   FILLING 

that  if  the  bulbous  portion  of  the  pulp  be  devitalized  by  cobalt  and 
removed,  leaving  the  root  portions,  the  latter  will  remain  vital  if 
protected  after  a  manner  described  by  him.  The  bulbous  portion 
of  the  pulp  is  cut  away  and  the  pulp  chamber  enlarged  by  means  of 
large  rose  burs.  Over  the  pulp  stumps  a  cylinder  of  tin-foil  is  laid, 
and  burnished  to  fit  the  floor  of  the  pulp  chamber  without  pressure 
upon  the  pulp  stumps  (Fig.  516) .    Over  this  a  filling  is  placed.    Herbst 

Fig.  516 


Herbst's  method  of  preserving  pulp  stumps. 

claims  that  the  pulp  stumps  will  remain  vital.  Were  this  to  be 
depended  upon,  it  would  be  a  marked  saving  of  time  and  trouble 
and  would  lessen  the  chances  of  pericementitis  subsequent  to  pulp 
removal;  but  when  it  is  known  that  the  cobalt  of  Herbst  is  metallic 
arsenic,  the  ultimate  death  and  decomposition  of  the  pulp  remnants 
seem  almost  inevitable,  and  in  fact  does  occur.  The  method  should 
not  be  employed. 

MUMMIFICATION   OF   THE   PULP. 

Many  experiments  have  been  performed  relative  to  leaving  in  sihi 
portions  of  pulps  and  covering  them  with  substances  having  for  their 
object  the  chemical  alteration  of  the  pulp  tissue,  so  that  no  peri- 
cementitis shall  result  from  its  putrefaction.  The  first  effort  in  this 
direction  is  credited  to  Witzel  in  1874. 

Miller,^  after  many  experiments  with  various  materials,  has  shown 
that  none  but  the  most  powerful  and  penetrating  antiseptics  have 
value  as  permanent  sterilizers.  These  are  the  cyanid,  bichlorid, 
and  salicylate  of  mercury,  sulphate  of  copper,  and  oil  of  cinnamon. 
Orthocresol,  carbolic  acid,  trichlorphenol,  and  zinc  chlorid  penetrate 
the  pulp  tissue  rapidly,  but  are  too  diffusible,  their  effects  disappear- 
ing in  a  few  weeks. 

He  classifies  salicylic  acid,  eugenol,  camphophenique,  hydro- 
naphthol,  ct-naphthol  and  /3-naphthol,  aceticotartrate  of  aluminum, 
and  some  essential  oils,  resorcin,  thallin,  sulphocarbolate  of  zinc,  etc., 
as  being  of  doubtful  value. 

1  Proceedings  of  Columbian  Dental  Congress,  1893. 


MUMMIFICATION  OF  THE  PULP  559 

Those  nearly  or  quite  worthless  are  iodoform,  basic  anilin  coloring 
matters,  borax,  boric  acid,  dermatol,  europhen,  calcium  chlorid, 
hydrogen  dioxid,  sozoiodol  salts,  tincture  of  iodin,  spirit  of  camphor, 
and  naphthalin. 

The  preparation  giving  the  best  results  consisted  of  mercuric 
chlorid,  0.0075  gram;  thymol,  0.0075  gram,  in  tablet  form. 

The  pulp  is  devitalized;  the  crown  portion  and  all  the  root  portion 
readily  accessible  are  removed;  one  of  the  tablets  is  placed  in  the  pulp 
chamber,  crushed  by  means  of  an  amalgam  plugger,  and  covered  with 
gold-foil.  The  mercury  salt  tends  to  discolor  the  crown  of  the  tooth, 
so  that  its  employment  should  be  restricted  to  the  posterior  teeth; 
indeed,  the  necessity  for  its  use  would  be,  as  a  rule,  found  with  these 
teeth,  being  those  from  which  it  is  most  difficult  to  extract  pulp 
remnants.  Miller  expresses  faith  in  the  power  of  oil  of  cinnamon  to 
permanently  sterilize  pulp  fragments. 

Soderberg^  recommended  a  paste  composed  as  follows: 

I^ — Alum  exsic, 
Thymol, 

Glycerol aa     3j 

Zinci  oxidi q.s.  to  make  a  stiff  paste — M. 

It  is  preferable  to  add  the  zinc  oxid  as  needed  or  to  make  a  small 
quantity  of  the  paste  frequently,  as  it  gradually  hardens.  To  the 
paste  used  a  crystal  of  cocain  is  added  to  prevent  pain.  Bennette,  of 
England,  has  advised  the  use  of  paraform  incorporated  in  the  paste, 
for  its  well-known  antiseptic  and  hardening  effects.  Greenbaiim 
suggested  the  use  of  a  drop  of  40  per  cent,  formaldehyd  solution  to  be 
incorporated  with  the  paste.  Both  reduce  the  pulp  to  the  consistence 
of  catgut. 

Soderberg  reopened  cases  months  after  application  of  the  paste  to 
pulp  stumps,  and  found  them  shrunken  and  with  an  odor  of  thymol 
about  them. 

He  applied  the  paste  in  the  manner  shown  in  Figs.  517  and  518. 
In  1900  Soderberg  reported  the  use  of  the  paste  in  about  900  cases, 
of  which  220  were  test  cases  of  from  two  to  six  years'  standing.  He 
claims  that  in  no  case  did  apical  pericemental  disturbance  arise 
from  the  use  of  the  paste  as  described. 

This  method  has  met  with  much  opposition  from  prominent  oper- 
ators, who  prefer  the  thorough  cleansing  and  filling  of  the  canals. 
No  doubt  the  rational  method  of  procedure  is  to  cleanse  the  canals 
as  well  as  possible,  and  to  use  the  paste  against  unremovable  pulp 
stumps. 

While  the  paste  may  effect  mummification  of  entire  canal  filaments 

1  Dental  Cosmos,  November,  1895. 


560     REMOVAL  OF  DENTAL  PULP  AND    ROOT-CANAL  FILLING 

of  pulp,  leakage  is  always  imminent  about  shrunken  pulps,  and  the 
only  safeguard  is  the  antiseptic  effect  of  the  paste.  This  is  much 
enhanced  if  the  bulk  of  putrefiable  material  be  replaced  with  the 
antiseptic  paste  used  as  a  root  filling.  Many  such  root  fillings  have 
done  good  service  for  many  years. 

Fig.  517  Fig.  518 


a,  caries  exposing  a  horn  of  the       a,  root  portion  of  pulp;  b,  mummifying  paste; 
pulp.  c,  zinc  phosphate;  d,  gold  or  amalgam. 

A  certain  percentage  of  failures  would  be  no  argument  against  the 
employment  of  the  method  when  indicated,  as  no  method  is  infallible 
in  all  circumstances,  and  particularly  in  those  in  which  the  present 
method  is  indicated. 

Pulp  Digestion. — Harlan  recommended  that  the  following  paste  be 
applied  to  unremoved  portions  of  dead  pulps  as  a  means  of  digesting 
them  preparatory  to  root  filling : 

I^ — Papain         gr-  v 

Price's  pure  glycerin TUiv 

Sol.  1  to  200  hydrochloric  acid lUv— M. 

This  is  applied  in  the  pulp  canal,  covered  with  blotting  paper 
soaked  in  liquid  vaselin,  and  the  whole  temporarily  sealed  for  a  few 
days.  The  pulp  is  reduced  to  the  consistence  of  jelly  and  can  be 
readily  washed  out. 

The  method,  on  the  whole,  does  not  seem  preferable  to  either 
mummification  or  the  Rhein  treatment  or  the  formocresol  treatment 
of  inextricable  portions  of  pulps  in  curved  roots,  etc.,  inasmuch 
as  the  occupancy  of  a  canal  by  a  sterile  pulp  remnant  is  better 
than  leaving  an  empty  root  canal  apex  or  filling  only  a  portion  of 
it  in  such  manner  as  to  render  subsequent  treatment  almost  im- 
possible. In  fact,  it  is  better  that  dentists  recognize  their  limitations 
and  put  themselves  in  position  to  do  future  good  to  the  patient, 
than  to  blindly  obstruct  efforts  in  that  direction. 

Perforations  and  Resorptions. — The  same  accidents  that  occur  in 
canal  opening  in  the  case  of  the  removal  of  anesthetized  or  devitalized 


MUMMIFICATION  OF  THE  PULP  561 

pulps  may  occur  in  all  gangrenous  cases  with  somewhat  increased 
UabiUty  to  infection  of  the  pericemental  tissue. 

In  old  cases  the  pericemental  tissue  may  hypertrophy,  causing  the 
condition  of  hyperplastic  (fungoid)  gum.  This  should  be  sterilized 
and  burned  away  with  the  electric  cautery  or  may  be  frozen  with 
ethyl  chlorid  and  ablated  with  sharp  instruments,  or  it  may  be 
saturated  with  trichloracetic  acid  and  ablated,  or  it  may  be  pressed 
away  (resorbed)  with  cotton  saturated  with  tincture  of  iodin  or  an 
antiseptic  oil.    The  perforation  is  then  covered. 

The  Filling  of  Perforations. — Perforations  made  high  up  in  the  canal, 
after  being  appropriately  sterilized  with  formocresol,  should  be  filled 
with  wax  or  with  gutta-percha  cones,  which  have  been  accurately 
fitted  to  the  openings.  It  is  often  difficult  to  do  this  accurately, 
but  the  effort  should  be  made.  When  ready,  a  little  antiseptic 
chloro-percha  is  to  be  placed  in  the  perforation  or  upon  the  cone, 
and  the  latter  packed  to  place. 

In  low  perforations  without  a  fistula  associated,  the  opening  of 
the  perforations  should  be  enlarged  inwardly  and  a  ball  or  plaque  of 
aseptic,  warm,  low-heat  gutta-percha,  or  even  temporary  stopping, 
adapted  to  the  opening.  A  piece  of  pure  gold  plate  may  be  burnished 
over  an  accessible  opening,  and  be  adapted  with  thick  chloro-percha 
or  temporary  stopping.  Any  of  these  may  be  fixed  in  place  with 
oxyphosphate  of  zinc.  Quick-setting  oxyphosphate  of  copper  in  its 
soft,  gummy,  state  may  be  painted  over  the  tissue  and  root  opening 
by  means  of  an  instrument,  or  the  perforation  may  often  be  satis- 
factorily closed  with  copper  amalgam.  When  in  posterior  teeth  a 
pin  must  be  used,  the  pin  may  be  made  smaller  than  the  root  canal 
and  be  coated  with  wax,  soft  oxyphosphate  of  copper  is  put  in  the 
canal,  and  the  pin  gently  thrust  in.  When  the  cement  has  set  the 
pin  may  be  heated  and  withdrawn,  and  when  included  in  the  intended 
superstructure,  the  pin  may  be  again  cemented  in  place  (see  Figs. 
378,  381,  and  382). 

When  a  perforation  threatens  to  produce  an  abscess  an  artificial 
fistula  should  be  made  and  the  case  treated  accordingly. 

If  a  perforation  have  a  fistula  associated  with  it,  the  oxyphosphate 
of  copper  or  zinc  oxychlorid  may  be  allowed  to  go  through  the  fistula, 
by  way  of  which  any  excess  may  be  removed. 

In  case  of  resorption  of  the  roots  of  permanent  teeth  great  difficulty 
may  present,  the  soft,  absorbent  tissue  having  grown  into  the  cavity 
in  the  root  side  which  it  has  made.  A  radiograph  will  aid  in  deter- 
mining the  extent  of  the  lesion,  which  usually  renders  canal  treatment 
impossible  and  extraction  imperative. 

36 


CHAPTER  XVIII. 
GANGRENE  OF  THE  PULP. 

Definition. — By  gangrene  of  the  pulp  is  meant  its  death  through  an 
interference  with  its  nutrition.  It  may  be  partial,  as  when  an  abscess 
in  the  pulp  or  violent  irritation  causes  the  bulbar  portion  to  die,  the 
canal  portions  being  found  alive;  or  when  only  one  canal  portion  is 
dead,  the  others  being  alive.    Either  dry  or  moist  gangrene  may  occur. 

Causes. — It  is  probable  that  a  construction  of  apical  root  tissue 
(hypercementosis)  about  the  pulp  may  so  constrict  it  as  to  bring 
about  its  death.  (For  the  primary  causes  of  this  see  Hypercemen- 
tosis.) Sudden  shocks,  such  as  occur  from  thread,  string,  or  cigar 
biting,  or  blows  or  rapid  movement  in  regulating  or  wedging,  or 
non-fixation  after  regulation,  may  cause  torsion  or  tension  of  the 
bloodvessels  entering  the  apex  of  the  pulp. 

These  influences  may  either  cause  pulp  hyperemia  or  strangulation 
of  the  apical  bloodvessels,  or,  possibly,  an  area  of  apical  thrombosis, 
cutting  off  the  nutritive  supply  to  the  pulp.  Septic  or  aseptic  inflam- 
mation of  the  pulp  may  cause  its  total  death.  Death  of  pulp  tissue 
due  to  arsenic  produces  results  in  nowise  differing  from  gangrene, 
provided  the  pulp  be  left  in  situ.    (See  p.  521.) 

DRY  GANGRENE   OF   THE   PULP. 

Definition. — By  dry  gangrene  of  the  dental  pulp  is  meant  its  death 
in  toto  and  its  subsequent  transformation  into  a  dry,  shrivelled  mass 
occupying  the  pulp  chamber  and  canal. 

Causes  and  Pathology. — If  the  pulp  die  and  remain  under  conditions 
which  exclude  bacteria  from  contact  with  it,  the  water  of  the  pulp 
may  be  removed,  leaving  the  organ  as  a  tough,  shrivelled  mass  (Fig. 
519).  The  conditions  most  favorable  seem  to  be:  (1)  Pulp  death 
from  some  aseptic  cause,  e.  g.,  the  hyperemia  resulting  from  a  blow 
on  a  sound  tooth;  (2)  constriction  of  the  apical  foramen,  due  to  hyper- 
cementosis, the  result  of  thread  biting  or  other  mild  irritation  of  the 
pericementum;  (3)  the  presence  of  secondary  dentin  over  the  bulbar 
portion  of  the  pulp,  causing  pulp  exhaustion  yet  protecting  it  from 
infection ;  (4)  the  capping  of  the  pulp  with  zinc  oxychlorid  or  f ormagen 
paste,  the  pulp  being  permeated  with  the  drug  or  dried  by  it;  (5)  the 
(562) 


DRY  GANGRENE  OF  THE  PULP  563' 

covering  of  pulp  stumps  with  a  paste  containing  a  tannifying  sub- 
stance, such  as  alum,  formaldehyde,  or  tannin. 

The  water  necessary  to  putrefaction  is  abstracted,  either  naturally 
or  chemically,  and  probably  bacteria  are  at  the  same  time  excluded, 
either  mechanically  or  because  the  chemical  substances  used  have 
penetrated  the  pulp  tissue,  acting  as  antiseptics. 

Symptoms. — The  tooth  has  a  nearly  normal  color,  but  under  a 
reflected  light  is  seen  to  have  lost  perfect  translucency.  There  is  no 
response  to  thermal  or  electric  tests  for  pulp  vitality.  The  dentin  is 
insensitive  to  cutting  instruments,  and  the  cuttings  upon  the  bur 
have  no  odor.  There  is  no  odor  or  fluid  in  the  pulp  canal  when  this 
is  entered,  and  the  pulp  is  found  as  a  tough,  dry  mass  not  unlike 
that  seen  in  a  dry  extracted  tooth  which  contained  a  vital  pulp  at 
the  time  of  extraction.  These  cases  as  spontaneous  occurrences  are 
relatively  rare. 

Tests  for  Pulp  Vitahty. — The  diagnosis  of  pulp  vitality  or  death 
being  in  practice  almost  daily  required,  the  decisive  tests  are  here 
indicated. 

A  tooth  containing  a  vital  pulp  is  translucent  and  pink;  that  con- 
taining a  dead  one  always  opaque  to  transmitted  light,  and  usually 
clouded  to  a  gray  or  bluish  black.  The  ordinary  appearance  by 
reflected  light  often  corresponds  to  this,  but  sometimes  a  tooth  is 
clouded  by  fillings,  or  looks  dead,  but  is  vital. 

An  electric  mouth  lamp  with  or  without  a  reflector  so  arranged  as 
to  reflect  the  light  upon  the  lingual  surface  of  the  tooth  will  supply 
the  means  for  this  test.  In  its  absence  strong  sunlight  may  be 
reflected  by  means  of  a  mouth  mirror,  but  is  not  nearly  so  good  a 
means  as  the  electric  light  (Fig.  369). 

If  the  tooth  be  isolated  by  means  of  rubber  dam  and,  first,  cold 
water  be  thrown,  or,  later,  ethyl  or  methyl  chlorid  be  sprayed  upon 
it  or  upon  the  filling  contained  in  it,  absence  of  response  will  indicate 
either  partial  or  total  pulp  death  or  the  formation  of  a  quantity  of 
secondary  dentin.  In  the  latter  case  the  test  must  be  renewed 
as  the  excavation  proceeds. 

A  hot  burnisher  or  hot  gutta-percha  applied  to  a  filling  or  dentin, 
or  very  hot  water  thrown  upon  an  isolated  tooth,  should  provoke  at 
least  a  delayed  response  from  a  vital  pulp. 

The  application  of  a  small  high  frequency  glass  electrode  to  the  tip 
of  a  vital  tooth  produces  a  peculiar  sensation  not  unlike  that  of 
hypersensitive  dentin.  It  is  due  to  the  fact  that  the  enamel  is  like 
glass  unable  to  insulate  the  high  frequency  current  which  passes  to 
the  dentinal  fibril.  A  devitalized  tooth  will  not  respond.  The 
facility  of  this  test  makes  the  apparatus  a  very  valuable  time  saver. 


564 


GANGRENE  OF  THE  PULP 


It  is  well  to  take  up  the  current  with  the  fingers  on  the  side  of  the 
tube  at  first  and  to  .raise  the  finger  after  the  glass  is  in  contact  with 
the  tooth. 

Woodward  has  shown  that  if  a  few  cells  of  a  cataphoric  apparatus 
are  in  action  and  the  positive  electrode  be  applied  to  the  dentin  or 
metal  filling  in  a  vital  tooth,  while  the  negative  pole  is  at  the  cheek 
or  wrist  of  the  patient,  a  distinct  sensation  should  be  felt,  while  in 
case  of  a  dead  pulp  there  will  be  no  response;  usually  even  a  small 
filling  will  transmit  a  distinct  shock  in  a  vital  tooth  which  is  absent 
in  a  devitalized  tooth.  A  mild  interrupted  current  has  also  been  used 
for  the  test.  There  may  be  no  response  through  a  metal  filling,  while 
such  response  may  be  obtained  by  packing  wet  cotton  against  the 
dentin  after  some  drilling.  A  mild  current  should  always  be  used 
unless  there  is  no  response,  when  the  strength  of  the  current  should 
be  increased.  It  is  generally  possible  to  test  some  evidently  vital 
tooth  nearby  as  a  control.  If  the  filling  reach  the  gum,  the  current 
may  be  transmitted  by  it.  The  possibility  of  contact  of  the  filling 
with  another  in  a  vital  tooth  is  to  be  remembered.  Insulation  with 
rubber  dam  is  indicated  in  such  a  case. 


F[G.  519 


Fig.  520 


Fig. 521 


Dry  gangrene  of  the 
pulp:  PN,  pulp  no- 
dule; DP,  shrivelled 
pulp.  (From  a  speci- 
men of  pulp  extracted 
intact  in  this  con- 
dition.) 


Caries;  moist  gangrene  in  impris- 
oned temporary  molar.  (Skia- 
graph by  Hagopian  from  editor's 
case.) 


Moist  gangrene. 
Skiagraph  of  unfilled 
root  canals  with  large 
mass  of  filling  mater- 
ial built  in  over  them. 
(Price.O 


In  doubtful  cases,  such  as  that  shown  in  Fig.  521,  the  .T-ray  skia- 
graph is  valuable,  and  indicates  at  least  the  removal  of  the  filling  for 
further  diagnosis  and  treatment.  When  dentin  is  insensitive,  pulp 
death  should  be  suspected. 

A  strong  odor  of  putrefaction  may  be  obtained  from  bur  cuttings 
in  cases  of  moist  gangrene  only.    This  must  be  differentiated  from 


1  Items  of  Interest,  1901. 


MOIST  GANGRENE  OF  THE  PULP  565 

the  odor  of  decayed  dentin,  which  usuall}-  also  has  an  acid  character. 
In  case  of  partial  death  of  the  pulp  not  discoverable  by  the  tests 
given  above,  a  fine,  sharp  probe  passed  into  contact  with  the  pulp 
remnant  will  demonstrate  its  vitality. 

Treatment. — If  septic  matter  be  introduced  a  violent  pericementitis 
may  be  lighted  up;  but  if  aseptic  precautions  be  employed  in  opening 
the  canal,  and  this  be  kept  under  the  influence  of  a  germicide,  such  as 
5  per  cent,  formaldehyde  or  sodium  dioxid,  the  root  may  be  filled. 
A  dressing  of  formocresol  may  be  introduced  for  a  time  and  the 
root  then  filled. 

A  temporary  filling  of  pink  base-plate  gutta-percha  is  to  be  inserted 
in  the  crown  cavity  until  all  irritation,  if  any,  subsides. 

Slight  aseptic  apical  irritation  may  be  anticipated  as  a  matter 
of  precaution  by  the  use  of  iodin  as  a  counterirritant  at  the  time 
of  root  filling  (see  p.  476).  Such  irritation  is  either  mechanical  or 
due  to  the  chemical  substances  used. 

MOIST  GANGRENE  OF  THE  PULP. 

Definition. — By  moist  gangrene  of  the  pulp  is  meant  death  of  pulp 
tissue  en  masse  and  its  subsequent  decomposition  by  the  action  of 
putrefactive  agencies.  As  putrefactive  decomposition  is  the  essential 
feature  in  these  cases,  and  that  which  gives  the  process  its  patho- 
logical significance,  the  causes,  nature,  effects,  and  treatment  of 
putrefactive  decomposition  of  the  pulp  are  included  under  this 
subheading. 

Causes. — The  causes  of  moist  gangrene  are  such  as  may  cause  the 
death  of  the  pulp  and  its  subsequent  decomposition  by  bacteria. 
Without  bacteria  putrefaction  cannot  occur.  Among  these  the 
Bacillus  gangrense  pulpse  (Arkovy)  figures  prominently.^  Four  types 
of  cases  are  seen:  (1)  In  teeth  apparently  sound;  (2)  in  teeth  filled, 
but  the  canals  not  treated — i.  e.,  death  of  the  pulp  has  occurred  after 
filling;  (3)  in  teeth  filled  with  canals  partly  filled;  (4)  in  teeth  having 
open  cavities  and  canals. 

In  the  first  type  of  cases  the  bacteria  may  enter  by  way  of  the 
blood  channels,  but  it  is  not  improbable  that  slight  cracks  or  histo- 
logical defects  in  the  enamel  may  admit  to  the  dentinal  tubules  the 
necessary  bacteria,  or  that  they  may  gain  entrace  by  way  of  the 
cementum  and  dentin  at  the  neck  of  the  tooth.  (See  Caush's  Tubes). 
The  inference  is  similar  in  case  of  trimmed  crowns  of  teeth  underlying 
gold  caps. 

1  Siberth  and  Goadby  regard  this  microorganism  as  a  variety  of  Bacillus  mesen- 
tericus,  probably  "niger."     Mycology  of  the  Mouth,  p.  148. 


566 


GANGRENE  OF  THE  PULP 


Pigment. 


Fig.  522 
Sulphur  +  hemoglobin. 


A  case  presenting  some  analogy  to  these  teeth  is  that  of  an  egg  with 
apparently  perfect  shell,  but  in  which  intense  decomposition  has 
occurred.  That  the  gases  and  other  odorous  products  are  somewhat 
confined  the  author  proved  to  his  dismay  as  a  boy  by  smashing  with 
a  hatchet  one  found  in  the  brush. 

Many  of  these  teeth  do  not  develop  abscesses  even  after  the  tooth 
has  become  dark  in  color;  perhaps  the  bacteria  are  killed  by  their 
own  products.    If  the  dentin  be  exposed,  as  at  the  incisal  edge,  the 

abscess  may  develop.  The  en- 
trance of  air  or  beginning  of 
treatment  often  starts  an  abscess 
unless  treatment  is  instituted. 

In  the  filled  cases  crevices 
about  crown  and  root  fillings 
may  admit  bacteria,  which  may 
pass  through  the  tubules  of  even 
secondary  dentin  in  some 
amount.  On  the  other  hand, 
it  is  irrational  not  to  admit  the 
possibility  of  an  infection  via  the 
circulation. 

In  cases  of  obvious  pulp  infec- 
tion beneath  fillings — e.  g.,  sup- 
puration of  the  pulp — the  bac- 
teria necessary  are  in  situ. 

In  the  open  cases  the  infec- 
tion obviously  arises  from  the 
mouth. 

Pathology  and  Morbid  Anatomy. 
— The  pulp  being  wholly  or 
partly  dead  from  any  cause 
whatever,  saprophytic  bacteria 
gain  access  to  it,  and  the 
serial  decomposition  it  under- 
goes is  in  exact  correspondence 
with  that  of  moist  gangrene  or  putrefaction  in  other  localities. 
In  this  serial  decomposition  albuminous  substances  are  first  trans- 
formed into  peptones  and  allied  substances,  some  of  them  being 
very  toxic.  Compound  ammonias,  known  as  ptomains,  or  animal 
alkaloids,  such  as  putrescin,  neuridin,  and  cadaverin,  are  probably 
next  formed.  Next  the  nitrogenous  bases — leucin,  tyrosin  (amido- 
acid),  and  the  amines  (methyl,  ethyl,  and  propyl) — make  their 
appearance,    together   with   organic   fatty    acids,      Next    aromatic 


CO2,  NH3; 

H2O  and  HsS. 


Aromatic  and 
fatty  prod- 
ucts. 

Ptomains. 


Peptones. 


Diagram  illustrating  the  more  com- 
plete decomposition  of  the  pulp  at  its 
coronal  end. 


MOIST  GANGRENE  OF  THE  PULP 


567 


products,  indol,  phenol,  cresol,  etc.,  and  finally  hydrogen  sulphid, 
ammonia  sulphid,  carbon  dioxid,  and  water.  By  alternating  pro- 
cesses of  hydration,  reduction,  and  oxidation,  bodies  of  increasing 
simplicity  of  chemical  composition  are  formed.    "Fermentation  and 


Fig.  523 


Fig.  526 


gflO  99«« 


Fig.  527 


Fig.  528 


7 


Fig.  529 


^^^ 


Fig.  530 


/•^ 


t 


putrefaction  can  only  occur  where  the  fungi  concerned  live  and  the 
extent  of  decomposition  is  conditioned  by  the  number  of  fungi. "^ 
The  contents  of  the  tubules   (fibrillse)   also    are  putrefied.     These 


Ziegler:  General  Pathology. 


568  GANGRENE  OF  THE  PULP 

products  ■  are  derived  from  the  following  chemical  constituents  found 
in  normal  pulps,  according  to  Hodgen:  Proteins  and  albuminoid, 
fibrin,  hemoglobin,  collagen,  elastin,  fats,  tripalmitin,  stearin,  and 
olein. 

The  irritant  bodies  are  probably  the  gases  and  ptomains  which 
have  experimentally  been  found  capable  of  producing  suppuration  in 
the  absence  of  bacteria. 

Miller^  found,  in  the  deepest  portions  of  the  degenerating,  putrefy- 
ing pulps,  where  inflammation  and  suppuration  were  in  progress  a 
preponderance  of  small  cocci  and  diplococci,  and  proceeding  toward 
the  open  pulp  chamber  an  increasing  number  of  large  cocci,  several 
forms  of  bacilli,  vibrios,  and  other  spirillse,  spirochetse,  and  long 
thread  forms  (Figs.  523  to  530).  Figs.  529  and  530  are  from  the  same 
pulp;  Fig.  524  was  taken  from  the  radicular  portion  of  a  pulp  which 
was  alive  and  suppurating;  Fig.  529  was  from  the  putrid  crown  por- 
tion. Miller  found  that  bacteria  of  pulp  putrefaction  cultivated  in 
gelatin,  with  and  without  the  access  of  air,  exhibited  a  difference  in 
the  poisonous  properties  of  their  products.  Those  developed  with 
free  access  of  air  produced  stronger  reaction,  and  more  extensive 
suppuration  than  those  developed  without  the  access  of  air. 

Arkovy,^  in  an  examination  of  43  cases  of  chronic  apical  abscess, 
pulp  gangrene,  etc.,  found  the  Bacillus  gangrense  pulpse  present  in 
41;  the  Staphylococcus  pyogenes  aureus  in  15;  Staphylococcus 
pyogenes  albus  in  8;  Staphylococcus  pyogenes  citreus  in  2;  Strepto- 
coccus pyogenes  in  10,  and  Bacillus  pyocyaneus  in  4. 

He  found  the  Bacillus  gangrense  pulpse  in  mouths  free  of  caries  as 
well  as  in  mouths  containing  carious  teeth,  and  established  the  fact 
that  it  is  pleomorphous  (bacillus  and  coccus  form). 

He  inoculated  healthy  pulps  with  this  bacterium,  and  found  that  in 
pure  culture  it  produced  total  gangrene  without  suppuration;  while 
mixed  cultures,  and  even  the  mixed  pleomorphic  forms  of  the  same 
bacillus,  produced  chronic  pulpitis. 

On  gelatin  cultures  a  putrid,  cheese-like  odor  was  perceptible.  The 
germ  is  subject  to  the  antiseptic  effects  of  strong  acids,  alkalies,  car- 
bolic acid,  and  tincture  of  iodin,  which  explains,  in  part,  the  success 
of  the  treatment  hereinafter  mentioned. 

Arkovy's  demonstration  seems  a  satisfactory  explanation  of  cases 
of  quiet  death  of  pulps  under  fillings. 

The  hydrogen  sulphid  combines  with  the  HN3  of  proteid  origin, 
to  form  ammonium  sulphid  (NH4)2S,  which,  again,  combines  with 
the  iron  in  the  hemoglobin  of  the  red  corpuscles,  producing  ferrous 

1  Dental  Cosmos,  1894. 

"  Synopsis  by  Soderberg:  Dental  Cosmos,  1899. 


MOIST  GANGRENE  OF  THE  PULP  569 

sulphid,  Fe2S,  which  darkens  the  decomposing  tissue,  and,  entering 
the  tubules,  stains  the  dentin  a  slate-gray  or  bluish-black  color. 
Other  derivatives  of  hemoglobin  may  be  responsible  for  the  yellowish 
brown  discoloration  often  seen  in  cases  in  which  bacteria  have  not 
reached  the  pulp  until  long  after  pulp  death.  The  color  is,  therefore, 
not  due  to  the  presence  of  hydrogen  sulphid. 

Miller"^  found  that  the  reaction  in  cases  of  putrefaction  was  alkaline 
unless  a  certain  percentage  of  sugar  was  introduced  into  the  medium, 
when  it  was  acid.  He  explains  the  voluminous  foul  odor  of  confined 
dead  pulps  as  due  to  the  absence  of  oxygen  of  air.  If  present  as  in 
open  pulp  cavities  the  gases  escape,  the  volume  being  therefore 
reduced,  oxidation  of  gases  increased,  and  an  acid  reaction  due  to 
entering  carbohydrate  permitted.  The  exact  nature  of  pulp  decom- 
position is  in  some  doubt. 

Fig.  522  is  a  diagram  illustrating  these  changes;  it  being  assumed 
that  the  decomposition  is  most  advanced  at  the  crown  portion  of  the 
pulp,  owing  to  the  entrance  of  bacteria  at  that  point. 

in  the  early  stage  of  the  process  the  gangrenous  pulp  resembles 
a  yellowish  mass  of  sloughing  tissue,  with  reasonably  tough  con- 
sistence, which  can  be  easily  removed.  In  the  later  stages  it  is  more 
decomposed  and  dark  and  jelly-like,  and  yields  to  the  broach. 
Naturally  the  greatest  number  of  fungi  will  have,  by  multiplication, 
invaded  and  putrefied  that  end  nearest  the  source  of  infection,  while 
the  more  consistent  (less  putrefied)  portion  of  the  pulp  will  exist 
at  the  apex.  In  the  final  stages  nothing  but  fluid,  or  even  an  almost 
dry  canal,  may  be  found.  This  last  condition  must  not  be  con- 
founded with  dry  gangrene.  If  fluid,  or  odor  without  fluid,  be 
present  the  case  is  one  of  moist  gangrene. 

Gangrenous  pulps  do  not  necessarily  produce  abscesses  at  once, 
but  often  clinical  history  shows  that  a  3'ear  or  two,  or  even  more, 
may  elapse,  though  as  short  a  time  as  two  or  three  weeks  has  some- 
times been  sufficient.  In  one  case  of  a  boy,  aged  ten  years,  the  time 
between  a  capping  of  a  bleeding  pulp  with  Jodoformagen  and  the 
presence  of  a  fistula  upon  the  gum  was  but  two  weeks.  It  was, 
however,  in  a  temporary  first  molar,  and  the  cement  covering  the 
cap  was  found  to  be  loose. 

The  forcing  of  gangrenous  pulp  tissue  by  instrumentation  into 
apical  tissue  generally  results  in  an  abscess,  even  when  extraneous 
bacteria  are  presumably  not  introduced. 

The  irritating  substances  in  a  decomposing  pulp  are  presumably 
the  bacteria,  the  ptomains,  and  the  expanding  gases. 

1  Microorganism  of  the  Human  Mouth,  1890 


570  GANGRENE  OF  THE  PULP 

Many  decomposed  pulps  produce  no  pain,  but  in  these  cases 
the  gases  may  escape  via  dentinal  tubules  and  leaks  about  fillings 
(Fig.  521). 

Clinically,  putrefactive  pulps  may  be  found  in  sound  teeth,  in 
filled  teeth,  and  in  teeth  the  pulp  cavities  of  which  are  open  to  the 
oral  fluids,  either  actually  or  through  the  medium  of  open  tubules 
in  the  dentin  over  them,  or  in  apical  portions  of  poorly  cleansed  or 
partly  filled  canals.  A  cotton  dressing  having  a  bad  odor,  or  an 
apparently  empty  apical  portion  of  canal  or  a  leaky  gutta-percha 
canal  filling  associated  with  a  bad  odor,  even  though  the  pulp  has 
been  successfully  removed,  have  a  similar  pathology.  There  is 
little  difference  in  principle  between  putrefactive  serum  or  tubule 
contents  and  a  putrefactive  pulp.  Any  of  these  may  cause  abscess 
or  remain  quiescent. 

Symptoms. — The  symptoms  are  opacity  of  the  tooth  evident  to 
the  eye  or  noted  by  transmitted  light,  bluish  or  brownish  discolora- 
tion of  varying  degrees,  odor,  and  discoloration  of  the  dentin  in  a 
cavity. 

There  is  a  lack  of  response  to  cutting,  thermal,  and  electric  tests. 
Sometimes  a  bad  taste  due  to  leakage  about  fillings  is  present.  Upon 
drilling  out  a  filling  the  odor  of  putrefaction  may  be  clearly  noticed 
even  before  entrance  of  the  canal,  and  sometimes  rises  to  the  operator's 
nostrils.  The  odor  of  the  bur  cuttings  is  diagnostic  in  less  pronounced 
cases.  The  gases  may  be  present  in  quantity  without  symptoms  of 
pain.  Looseness,  tenderness  to  percussion,  incipient  and  acute 
abscess,  or  a  chronic  fistula  are  evidences  of  pericemental  irritation. 

Pain  to  heat,  while  usually  indicative  of  pulp  irritation,  also  some- 
times occurs,  and  is  explainable  upon  the  same  theory  of  the  expan- 
sion of  gases  against  vital  tissue — in  this  case  the  apical  tissue.  These 
symptoms  are  all  explained  by  the  pathology  of  the  condition. 

A  confusing  condition  clinically  is  found  where  one-half  of  a  pulp 
has  died  and  undergone  decomposition,  as  in  molars,  the  other  half 
remaining  vital,  although  the  seat  of  infection  and  inflammatory 
action.  So  far  may  this  condition  go,  that  abscess,  acute  or  chronic, 
may  be  present  upon  the  root  of  one  tooth  long  before  the  second 
segment  of  the  pulp  has  succumbed.  The  diagnosis  of  such  cases  is 
made  by  the  light  test,  by  obtaining  the  painful  reaction  to  heat  and 
perhaps  to  electricity,  and  usually  some  tenderness  upon  percussion 
upon  some  particular  portion  of  the  tooth;  upon  opening  the  tooth 
the  peculiar  condition  described  is  found.  The  .T-rays  should  show 
the  condition. 

In  one  case  of  a  lower  molar  with  a  fistula  related  with  the  distal 
root  I  found  the  pulp  apparently  vital  upon  entering  the  pulp  chamber 


MOIST  GANGRENE  OF  THE  PULP  571 

with  a  bur  at  a  point  about  midway  between  the  horns.  There  was 
apparently  a  persistence  or  hypertrophy  of  the  pulp  bulb  attached  to 
the  mesial  filaments.  The  distal  canal  was  found  to  contain  only  the 
fluid  remains  of  a  dead  pulp  filament.  In  cases  seen  at  the  right 
time  the  bulbal  half  of  a  pulp  may  be  gangrenous  without  positive 
putrefaction,  while  the  apical  half  is  still  vital. 

J.  H.  McQuillen^  recorded  a  case  of  longitudinal  fracture  of  a 
bicuspid  tooth  extending  from  the  sulcus  to  the  bifurcation  of  the 
roots,  and  which  was  apparently  due  to  the  expansion  of  the  gases 
of  decomposition.  Poinsot^  records  a  similar  case,  and  states  that 
several  teeth  containing  decomposed  pulps  confined  in  a  glass  tube 
caused  the  latter  to  break. 

Fig.  531 


Tooth  split  by  gas.     (Roff.) 

Dr.  S.  H.  Roff,^  of  Cincinnati,  Ohio,  has  presented  the  case  shown 
in  Fig.  531.  He  had  it  under  observation  for  seven  years.  He 
regarded  the  case  as  one  of  slow  progressive  cracking  (a  run)  with 
final  irritation  and  death  of  the  pulp  and  the  final  clean  longitudinal 
fracture  as  due  to  the  gases  from  the  partially  decomposed  pulp. 
When  one  considers  the  fact  that  wet  plugs  of  soft  wood  will  split 
granite  boulders  we  must  accept  the  possibility  of  tooth  fracture 
by  gas  pressure. 

Observations  previous  to  that  of  McQuillen  have  recorded  a  sound, 
as  of  an  explosion,  to  have  occurred  simultaneously  with  the  fracture 
of  the  tooth.  I  have  looked  all  my  professional  life  for  such  a  case, 
but  though  I  have  seen  quite  a  number  of  clean  fractures  I  have 
never  been  able  to  eliminate  the  possibility  of  fracture  from  ordinary 
causes  and  in  some  of  the  cases  have  had  positive  histories  of  direct 
violence. 

Treatment. — The  pulp  being  presumably  infected,  all  quiescent 
gangrenous  pulps  or  putrefactive  conditions  under  any  conditions 

1  Dental  Cosmos,  1871.  2  Ibid.,  1901. 

3  Items  of  Interest,  March,  1912. 


572  GANGRENE  OF  THE  PULP 

discovered  indicate  a  similar  treatment,  namely,  first  disinfection  to 
remove  or  kill  bacteria  which  might  cause  an  abscess  and  at  the 
same  time  to  destroy  the  chemical  nature  of  the  gases  and  ptomains. 
After  this  the  canals  are  to  thoroughly  opened,  cleansed,  further 
disinfected  for  the  sake  of  surety,  and  later  filled. 

Three  substances  are  preeminent  in  this  direction — (1)  formal- 
dehyd,  (2)  nascent  oxygen,  (3)  iodin  or  its  derivatives. 

At  the  present  writing  no  substance  equals  formaldehyd,  because 
of  its  rapid  diffusion  as  a  gas  through  all  canals,  tubules,  and  even 
abscess  tracts. 

The  first  and  best  treatment  consists  in  opening  the  pulp  cavity  and 
gently  removing  the  bulk  of  decomposed  pulp  from  the  pulp  chamber 
and  canals,  care  being  employed  to  avoid  forcing  any  putrid  material 
into  the  apical  tissue  by  broaching  or  plunging  of  the  bur.  Also,  no 
bacteria  should  be  introduced  from  outside.  The  opening  should  not 
be  too  freely  made,  and  should  be  funnelled  or  countersunk  out- 
wardly to  secure  the  seal  against  being  plunged  into  the  pulp  cavity 
in  mastication  (Fig.  532). 

This  being  done,  the  canals  are  dried  with  cotton  and  hot  air,  and 
a  small  pellet  of  cotton  saturated  with  formocresol  or  10  per  cent, 
aqueous  formaldehyde  solution,  or  geranium  formol^  is  to  be  placed 
in  the  pulp  chamber. 

I^ — Formaldehyd 40  parts 

Essence  of  geranium,  distilled 20  parts 

Alcohol  80  per  cent 40  parts 

Any  that  has  come  in  contact  with  the  orifice  should  be  removed 
with  alcohol.  The  orifice  is  then  dried  and  a  small  piece  of  dry  spunk 
placed  over  the  application,  but  not  so  as  to  interfere  with  the 
seal.  Quick-setting,  adhesive,  hydraulic  cement  is  now  flowed  into 
the  orifice,  air  bubbles  being  avoided  by  flowing  it  in  with  an  instru- 
ment (Fig.  532) .  A  bit  of  paraf orm  accomplishes  the  same  purpose 
as  the  solution,  namely,  the  liberation  of  formaldehyd  gas. 

When  opportunity  for  self-relief  seems  proper,  as  when  the  operator 
is  leaving  his  practice  for  a  short  time,  or  may  otherwise  be  inacces- 
sible, hot  temporary  stopping  may  be  used  and  the  patient  instructed 
as  to  the  proper  procedure  to  obtain  relief.  An  ordinary  pin  crooked 
at  the  point  by  striking  it  across  any  hard  surface  will  serve  to  pick 
out  the  stopping  and  cotton.  In  all  cases  tight  coverings  must  be 
made,  as  the  object  is  to  concentrate  the  action  of  the  formaldehyd 
gas  upon  the  canal  and  tubular  contents. 

In  some  cavities  it  is  well  to  make  the  covering  first,  as  done  for 

1  Geranium-formol  introduced  by  Andre  and  de  Marion,  I'Odontologie;  abstract 
by  International  Dental  Journal,  1901. 


MOIST  GANGRENE  OF  THE  PULP 


573 


arsenic  (see  Fig.  453),  and  to  seal  the  dressing  in  with  a  further 
addition  of  cement  or  temporary  stopping.  The  latter  does  not 
permit  mastication  like  the  former. 


Fig.  532 


Fig.  533 


a,    cotton    and    formocresol;   b,  spunk; 
c,  cement. 


Cervical  wall  built  up  with  amal- 
gam to  permit  canal  sterilization 
and  treatment. 


If  there  be  a  broad  cavity  extending  beneath  the  gum,  it  is  well 
to  press  the  gum  away  with  cotton  pellets,  then  to  form  the  cavity 
and  open  the  canal  orifices.  Then  a  retention  at  the  cervical  portion 
of  the  cavity  should  be  made,  even  if  it  be  necessary  to  drill  a  series 
of  pits  along  it  with  a  No.  1  bur.  Spunk  is  now  placed  over  the 
pulp  canals  and  quick-setting  amalgam  is  to  be  permanently  built 
in  at  this  part  of  the  cavity.  When  set  the  spunk  is  withdrawn, 
formocresol  in  cotton  is  placed  instead  of  the  spunk,  and  the  covering 
completed  with  cement.  The  amalgam  is  finished  as  far  as  practi- 
cable at  the  one  sitting,  and  the  case  dismissed.  At  future  sittings 
the  rubber  dam  may  be  applied  and  the  canal  work  done  (Fig.  533). 
When  cavity  walls  are  frail,  spunk  may  be  placed  in  the  pulp  cavity, 
and  a  permanent  cement  lining  built  into  the  cavity.  This  can  be 
perforated  to  the  spunk,  thus  leaving  the  walls  supported  during 
the  treatment. 

Formocresol,  introduced  by  Buckley,  consists  of  equal  parts  of  37 
per  cent,  aqueous  formaldehyd  solution  and  cresol,  which  combine 
well. 

According  to  Buckley,  the  formaldehyd  not  only  acts  as  a  germi- 
cide, but  combines  with  the  ammonia  of  ammonium  sulphid  to  form 
urotropin  and  water,  6CH2O  +  4NH3  =  (CH2)6N4  +  6H2O,  and 
with  hydrogen  sulphid  to  form  sulphur  and  methyl  alcohol,  2CH2O  + 
2H2S  =  82  +  2CH3OH.  The  cresol  is  supposed  to  act  upon  the 
fatty  compounds,  changing  them  into  a  compound  resembling  lysol. 
Thus,  antiseptic  substances  are  formed  from  poisonous  ones.  This 
does  not  necessarily  represent  all  the  reactions  occurring,  as  many 
other  compounds  may  result  from  putrefaction.    The  probability  is 


574  GANGRENE  OF  THE  PULP 

that  the  thoroughly  bactericidal  action  is  the  one  of  greatest  value. 
This  action  has  been  shown  by  Mayrhofer  to  be  true  only  for  the 
first  twenty-four  hours;  thereafter  the  bacteria  in  the  tubules  may 
grow  back  into  the  canal  and  the  dressing,  in  spite  of  the  fact  that 
the  odor  of  the  dressing  is  present.  The  canal  should  therefore  be 
mechanically  cleaned  after  twenty-four  hours,  and  a  fresh  application 
be  made.i  Mayrhofer  claimed  inability  to  sterilize  permanently 
with  formocresol.  Nevertheless  the  editor  treats  such  cases  at  wide 
intervals  ordinarily  with  impunity.  In  a  few  cases  an  abscess  has 
supervened  after  the  first  dressing,  but  none  as  yet  after  the  second. 
Leakage  of  the  formaldehyd  gas  may  have  been  the  reason,  but  a 
chronic  apical  abscess  in  the  third  stage  (which  see)  has  been  a 
suspicion.  Cleansing  and  reaming  the  canals  at  the  first  sitting  is 
another  danger,  even  when  formaldehyd  is  subsequently  used.  This 
must  sometimes  be  done  as  when  a  crown  is  broken  away  and  the 
root  canal  is  foul. 

Formaldehyd  is  so  efficacious  in  the  writer's  hands  that  it  has 
displaced  other  methods  in  his  practice.  All  other  methods  of 
disinfection  produce  results  less  certain  than  those  produced  by  it, 
and  are  more  cumbersome,  therefore  they  will  be  here  dispensed 
with.  While  this  is  true  for  a  great  majority  of  the  cases,  occasionally 
a  patient  is  met  with  whose  tissues  do  not  tolerate  formaldehyd 
well.  Formocresol  then  should  be  reduced  to  a  5  per  cent,  solution 
with  cresol  or  phenol  camphor,  and  in  some  cases  abandoned  for 
more  sedative  antiseptic  remedies,  such  as  eugenol  or  phenol  camphor 
with  menthol  or  thymol  or  iodoform  may  be  tried. 

This  first  dressing  may  be  left  for  from  twenty-four  hours  to  a  week 
or  longer  if  the  patient  is  comfortable. 

At  the  second  sitting  the  rubber  dam  is  to  be  applied  and  the  canal 
opening  thoroughly  made  under  formocresol  influence,  just  as  though 
the  pulps  were  vital,  the  technique  differing  in  no  respect.  (See 
pp.  532  to  548.)  A  second  dressing  is  introduced  into  the  canals. 
Whether  this  shall  carry  the  full  strength  formocresol  or  it  shall  be 
modified  by  the  addition  of  cresol  or  phenol  camphor  depends  upon 
the  history  of  any  irritation  or  perfect  comfort  as  a  result  of  the 
first  application.  The  object  of  a  second  dressing  is  to  determine 
whether  the  odor  (gases)  has  been  discharged  from  the  tubules. 
When  the  dressing  has  absence  of  putrefactive  odor,  no  pus  can 
be  detected,  and  the  patient  is  comfortable,  the  canal  is  ready  for 
filling.  Less  than  this  result  is  too  soon,  and  delay  beyond  this  is 
a  loss  of  time. 

1  ViuUeumier:  Items  of  Interest,  March,  1910. 


MOIST  GANGRENE  OF  THE  PULP  575 

When  one  pulp  filament  is  gangrenous  and  another  vital,  the  treat- 
ment is  the  same,  it  being  the  writer's  experience  that  formocresol 
loosely  placed  is  not  incompatible  with  ulcerated  pulps,  and,  indeed, 
is  an  excellent  dressing  for  suppurative  pulps  when  modified  to  a  3 
to  5  per  cent,  strength;  even  full  strength  has  been  acceptably  used. 
Later,  the  vital  portion  is  appropriately  removed. 

When  apical  pericementitis  of  a  subacute  nature  is  present  on  a 
filled  tooth,  as  when  a  tooth  shows  some  looseness  and  tenderness, 
with  some  injection  of  the  gum,  all  faulty  root  canal  fillings  should 
be  removed  with  barbed  broaches,  cleansers,  or  root  reamers,  and 
the  case  is  then  resolved  into  one  of  moist  gangrene  and  treated 
accordingly. 

Wax  may  be  removed  by  over  heating  with  the  hot  root  drier  and 
absorption  with  cotton,  or  oil  of  cajeput  may  be  used  as  a  solvent. 
Paraffin  may  be  removed  in  like  manner,  xylol  is  a  solvent. 

If  a  cotton  root  filling  be  found  it  sometimes  allows  the  broach  to 
tear  loose.  In  such  case  a  Kerr  broach  is  driven  into  it  to  create 
a  central  opening,  after  which  the  fibres  become  engaged  by  the 
barbed  broach. 

Eucalyptol  or  chloroform  may  be  used  to  soften  gutta-percha  root 
canal  fillings,  and  at  times  the  smallest  Kerr  or  Downie  broach  is  to 
be  bibevelled  at  its  end  and  used  as  a  drill,  cutting  its  way.  Oxy- 
chlorid  and  other  cement  fillings  may  have  50  per  cent,  sulphuric  acid 
or  strong  ammonia  water  applied  to  them  to  assist  in  breaking  up 
the  bond  of  the  cement  by  chemically  destroying  either  the  zinc 
oxid  or  the  acid.  The  drill  will  tamp  the  fluid  into  the  cement 
and  cut  the  cement  at  the  same  time. 

All  root  fillings  of  cement  nature  are  apt  to  be  faulty  when  used 
as  such,  because  the  air  in  the  canal  prevents  ingress,  though  it 
may  appear  to  be  well  filled.  This  fact  is  of  importance  in  diagnosis 
in  filled  teeth,  giving  evidence  of  chronic  pericementitis,  i.  e.,  there 
is  probably  an  unfilled  portion  of  root  canal  containing  putrefied 
pulp  or  serum. 

It  is  a  weakness  of  many  good  operators,  if  not  all,  to  think  that 
their  individual  canal  fillings  are  perfectly  made.  The  writer  was 
once  associated  with  a  most  conscientious  man,  and  possesses  a  gutta- 
percha canal  filling  of  his  in  a  molar  now  successful  for  twenty  years. 
On  one  occasion  he  declared  that  he  had  filled  perfectly  a  canal  of 
an  upper  second  bicuspid,  because  the  material  had  been  felt  by  the 
patient  as  it  reached  the  apex.  Two  weeks  later  the  tooth  was 
extracted,  though  comfortable,  for  orthodontic  purposes.  Its  well- 
opened  canal  was  empty  for  a  quarter  of  an  inch  at  the  apex. 

To  remove  pins  from  roots  a  bibevelled  Kerr  broach  may  be  driven 


576  GANGRENE  OF  THE  PULP 

into  the  cement  or  dentin  about  it  and  the  drifts  united.  The  pin 
may  often  be  forced  to  one  side  and  then  jigged  loose.  If  there  be 
sufficient  pin  extending  above  the  face  of  the  root  a  "pin  puller" 
may  be  used.  If  the  pin  cannot  be  loosened  it  must  be  drilled  out 
bodily.  A  sharp  round  bur  should  be  used  to  countersink  the  end  of 
the  pin,  and  then  by  the  aid  of  oil  it  is  cut  into  shavings.  Frequent 
desiccation  and  examination  to  observe  the  presence  of  a  metal 
remnant  is  necessary  to  avoid  the  accident  of  perforation. 

In  drying  with  the  compressed-air  syringe,  care  should  be  employed 
to  avoid  extensive  emphysema  of  the  cheek,  which  may  be  induced 
by  intense  pressure.  If  it  occur,  the  emphysema  should  be  reduced 
by  manipulation,  with  a  view  to  gently  forcing  the  air  back  through 
the  root.  Christensen^  and  L.  Greenbaum  have  each  reported  a 
case,  and  the  editor  had  his  first  case  when  desiccating  an  accidental 
lateral  perforation.  This  occurred  even  without  close  application 
of  the  syringe  nozzle,  35  pounds  pressure  being  used. 

Another  case  occurred  while  an  upper  lateral  with  large  apical 
foramen  and  even  with  an  open  fistula  was  being  dried  out.  The 
entire  right  cheek  and  lower  eyelid  was  instantly  puffed  up.  The 
patient  called  attention  to  a  stiffness  and  coldness.  It  subsided 
upon  manipulation.  There  might  be  dangerous  sequelae  if  sepsis  were 
present. 

The  immediate  treatment  of  canals  containing  gangrenous  pulps 
may  at  times  be  necessary.  The  mechanical  work  should  be  done 
while  the  canal  is  flooded  with  formocresol,  and  embalming  paste 
containing  paraform  should  be  used  with  gutta-percha  canal  points, 
or  sometimes  on  cotton  twists. 

If  any  inaccessible  portion  of  root  canal  remain  it  may  be  treated 
according  to  Rhein's  method.     (See  p.  539.) 

Root  sterilization  may  be  immediately  attempted  after  the  rubber 
dam  has  been  placed  and  the  crown  washed  with  5  per  cent,  formalin 
or  alcohol  and  water. 

A  little  dry  sodium  dioxid  is  placed  upon  a  slab  with  a  drop  of 
water  near  it.  A  broach  is  drawn  through  the  water,  then  through 
the  powder,  and  the  adherent  powder  carried  to  the  canal  and  gently 
passed  into  the  moist  putrid  contents  of  the  canal;  a  reaction  occurs 
between  the  water  and  sodium  dioxid  as  follows:  Na202  +  2II2O  = 
H2O2  +  2NaOII,  producing  hydrogen  dioxid  and  sodium  hydrate. 

The  sodium  hydrate  or  lye  saponifies  all  fatty  matters  and  destroys 
organic  matter,  even  living  matter,  aiid  the  hydrogen  dioxid  liber- 
ates nascent  oxygen,  which  is  a  disinfectant.     No  oil  or  phenol 

1  Dental  Cosmos,  1904,  p.  151. 


MOIST  GANGRENE  OF  THE  PULP  577 

should  be  used  with  dry  sodium  dioxid,  as  an  explosion  may  occur. 
The  use  of  the  alloy  kalium  natrium  in  a  moist  canal  causes  an 
oxidation  of  the  metals  by  the  O  of  the  water,  flame  being  the  result 
of  ignition  of  the  hydrogen.  Sodium  and  potassium  hydrate  are 
formed. 

The  result  of  the  reaction  should  be  washed  out  with  a  gentle 
stream  of  warm  water,  while  a  broach  is  gently  passed  to  and  fro 
through  the  mass.  The  action  is  then  repeated  as  far  as  it  can  be 
carried. 

The  danger  in  the  use  of  these  materials  lies  in  the  possibility  of 
the  production  of  a  chemical  inflammation  of  the  apical  tissue,  due 
to  the  nascent  hydrates,  if  the  foramen  be  open,  which  inflammation 
may  be  severe,  or  in  the  possibility  of  a  non-sterilization  of  the 
contents  of  inaccessible  canals.  For  this  reason  it  may  be  well  in 
fine  roots  to  follow  with  the  Rhein  method,  or  to  use  a  formalin 
solution  for  the  purpose  of  completing  the  sterilization  in  the  more 
open  roots,  and  20  per  cent,  formalin  or  25  per  cent,  ethereal  pyro- 
zone  (H2O2)  for  the  finer  roots. 

Following  this  the  root  filling  is  either  attempted  immediately 
with  removable  antiseptic  root  fillings  or  a  dressing  of  5  per  cent, 
formalin  introduced  into  the  dried  canal  for  a  few  days. 

Any  irritation  of  chemical  nature  may  be  treated  in  anticipation  by 
the  use  of  counterirritants  applied  to  the  gum.  While  this  may  be 
done  in  some  cases  the  occasional  production  of  an  abscess  leads  the 
editor  to  strongly  advise  the  first  treatment  suggested.  The  writer 
on  a  Monday  lanced  an  acute  abscess  on  a  cuspid  treated  with  kalium 
natrium  by  a  clinician  at  a  clinic  on  Saturday.  Opening  the  canals 
under  antisepsis  with  formocresol  kept  in  them  while  broaching, 
etc.,  is  an  even  better  immediate  method,  but  still  not  so  good  as 
twenty-four  hours'  sterilization,  then  free  opening. 

The  filling  of  canals  by  driving  wood  points  saturated  in  carbolic 
acid  into  the  infected  canals,  forcing  carbolic  acid  by  pressure  into 
the  apical  tissue,  and  the  filling  with  gutta-percha  are  all  successful 
in  many  cases;  but  there  is  much  likelihood  of  apical  abscess,  or,  at 
least,  of  traumatic  or  chemical  irritation,  which  it  requires  much 
courage  not  to  undo,  with  a  patient  complaining,  and  some  doubt  as 
to  whether  an  abscess  will  result,  so  that  more  gradual  yet  thorough 
work  is  advisable,  at  least  for  the  young  practitioner  who  must 
retain  the  confidence  of  the  patient. 

Hoffendahl,^  of  Berlin,  has  extended  the  demonstration  of  Zierler 
and  shown  that  the  constant  galvanic  electric  current  from  a  battery 

1  Dental  Cosmos,  1905. 
37 


578  GANGRENE  OF  THE  PULP 

of  from  30  to  40  Leclanche  cells  to  overcome  the  resistance  of  the 
tissues  will  electrolytically  decompose  0.75  per  cent,  sodium  chlorid 
solution  and  drive  nascent  chlorin,  H2O2,  and  oxygen  through  even 
fine  root  canals  and  into  the  infected  tissue  about  an  abscess  cavity. 
Thus,  electrolysis  and  cataphoresis  are  brought  into  play.  The 
current  does  not  pass  through  the  side  of  the  root;  a  street  or  central 
direct  current  with  a  rheostat  attachment  reducing  the  current  to 
from  0  to  80  volts  is  equally  effective. 

The  tooth  should  be  rubber  dammed  to  insulate  the  gum.  The 
canal  should  be  carefully  cleansed,  so  as  not  to  permit  ptomains  to 
pass  into  the  apical  tissues,  and  then  filled  with  a  sodium  chlorid 
solution.  A  fine  platinum  electrode  is  introduced  into  the  moist 
canal,  and  must  be  attached  to  the  positive  pole  of  the  battery.  A 
large  moist  negative  electrode  is  to  be  applied  to  the  hand  to  lessen 
resistance  and  conduct  the  current  to  the  negative  pole  of  the  battery. 
The  size  prevents  uncomfortable  sensations  about  the  tooth.  The 
rheostat  should  be  manipulated  so  as  to  introduce  the  current  gradu- 
ally until  about  1.5  mi.  is  recorded  on  the  meter,  and  should  be 
continued  for  five  minutes.  An  antiseptic  dressing  is  then  inserted, 
and  a  few  days  later  the  current  is  repeated  to  destroy  any  bacteria 
developed  in  the  interim,  when  the  root  may  be  filled.  Hoffendahl 
employs  a  paste  of  paraform,  thymol,  oil  of  cloves,  and  zinc  oxid 
packed  by  means  of  asbestos  fibres. 

In  experiments  in  conjunction  with  W.  D.  Miller  they  found  0.6 
mi.  passed  for  ten  minutes  through  a  putrid  pulp  to  which  pure 
cultures  of  germs  were  added,  sterilized  the  pulp  so  that  agar  cultures 
failed ;  canals  of  multirooted  teeth  are  best  treated  separately. 

The  principle  involved  in  immediate  sterilization  is  the  destruction 
of  all  septic  matter  within  the  canal  and  beyond  the  apex  at  the 
first  sitting. 

After  the  canal  disinfection  is  accomplished  by  one  or  more  of  the 
various  immediate  means  suggested,  its  walls  should  be  desiccated 
and  made  absorbent  by  means  of  hot  air,  then  moistened  with  euca- 
lyptol  or  forma-percha,  and  a  root  filling  of  temporary  stopping  or 
gutta-percha  packed  in.  If  aristol  be  added  to  these  the  effect  is 
increased.  Cotton  and  formo-percha  make  a  readily  removable 
filling  suitable  to  cases  in  which  some  doubt  exists.  I  have  had 
excellent  results  in  molars  with  this  material.  (See  p.  551.)  A  tem- 
porary filling  of  base-plate  gutta-percha  is  then  placed  in  the  crown 
cavity  as  a  test  filling,  or,  in  case  of  need,  the  filling  may  be  inserted. 

Any  apical  irritation  may  be  attributed  to  the  disinfectant  and  be 
treated  by  counterirritation,  or  the  counterirritant  may  be  applied 
as  a  precaution  at  tHe  time  of  operation.    Refrigeration  of  the  gum 


MOIST  GANGRENE  OF  THE  PULP  579 

over  the  root  by  means  of  ethyl  chlorid  is  a  valuable  means  of  reduc- 
ing inflammation  in  these  cases.  This  traumatic  irritation  is  often 
mistaken  for  acute  septic  pericementitis.  Any  irritation  not  too 
severe  is  to  be  considered  as  due  to  non-septic  causes  and  treated 
accordingly.  A  few  of  these  cases  may,  of  course,  result  in  failure 
owing  to  imperfection  in  the  application  of  the  method.  The  great 
majority  of  cases  are  successful.  Still,  if  one  desire  still  fewer  failures, 
employ  the  first  method. 

The  withdrawal  of  the  cotton  dressing  in  the  tentative  method 
should  be  done  under  aseptic  precautions.  There  may  be  found  no 
collection  upon  cotton.  In  such  case  a  fresh  twist  on  a  Swiss  broach 
should  be  passed  to  the  apex  to  determine  its  condition.  If  nothing 
be  found  the  root  may  be  dried  and  filled  unless  odor  be  present, 
when  the  root  should  be  resterilized  before  filling,  or  the  dressing 
renewed. 

Active  hemorrhage  may  ensue  or  serum  may  ooze  from  the  apical 
tissue.  This  may  be  checked  with  25  per  cent,  pyrozone,  adrenalin 
chlorid,  1  to  1000,  or,  preferably,  alum  and  thymol,  and  the  root 
filled. 

If  the  apical  foramen  be  a  large  one,  and  if  a  pus  flow  follow  the 
removal  of  the  temporary  dressing  and  be  but  slight,  the  pyrozone 
or  zinc  chlorid  (or  both)  should  be  used  and  the  root  filled.  The 
condition  is  one  of  apical  abscess  without  fistula,  and  is  often  amen- 
able to  immediate  root  filling.  If,  however,  this  be  not  considered 
advisable,  the  temporary  dressings  may  be  renewed,  though  often 
without  benefit.  Sometimes  a  thick,  glairy  fluid  will  ooze  from  the 
apical  tissue.  This  is  coagulable  lymph,  and  the  parts  require 
treatment  in  the  same  manner  as  when  a  slight  amount  of  pus  is 
present.  The  principle  involved  in  the  departure  to  an  immediate 
method  of  treatment  is  based  upon  the  thorough  sterilization  of 
the  apical  tissue,  the  sealing  of  the  canal  to  prevent  infection  from 
the  mouth,  and  the  prevention  of  effusions  from  the  apical  tissue 
into  the  canal.  This  done,  the  apical  tissue  is  expected  to  care  for 
itself. 

In  order  to  prevent  apical  irritation  in  so  far  as  possible,  the  gum 
is  to  be  painted  with  ordinary  tincture  of  iodin  or  spotted  with  the 
dental  tincture  of  iodin,  both  lingually  and  buccally,  as  a  counter- 
irritant. 

I^ — Iodin 5iij 

Alcohol Sj 

Shake  frequently  for  a  week  or  two.     (Flagg.) 

If  infection  of  the  apical  tissue  by  any  chance  ensue,  either  as  the 
result  of  the  operation  of  canal  cleansing  or  previous  to  operative 


580  GANGRENE  OF  THE  PULP 

interference,  the  disease  known  as  septic  apical  pericementitis  is 
established. 

Pericementitis  following  the  opening  of  teeth  containing  gangrenous 
pulps  has  been  explained  upon  the  ground  that  the  bacteria  in  the 
absence  of  free  admission  of  oxygen  have  lost  their  virulence,  which 
is  restored  when  the  air  is  admitted.  It  is  quite  likely  that  either 
this  is  true  or  that  extraneous  bacteria  are  introduced  during  the 
course  of  treatment. 

In  case  of  partial  moist  gangrene  in  which  a  portion  of  a  filament 
is  gangrenous  and  the  balance  of  it  vital,  or  in  which  one  root 
filament  is  dead  and  the  other  vital,  the  treatment  must  be  varied 
to  suit  the  requirements.  The  dead  portion  is  removed  as  described 
and  the  living  portions  treated  as  ulcerated  pulps.     (See  p.  496.) 

In  a  few  cases  the  continuity  of  the  canal  has  been  lost  because  it 
has  become  involved  in  caries  upon  one  side  of  the  root.  This  may 
be  treated  as  described  on  p.  432. 

Discoloration  of  the  Teeth  by  Moist  Gangrene. — In  the  final  decom- 
position of  the  pulp  a  pigment  molecule  is  formed,  which,  entering 
the  tubules  or  formed  in  it,  stains  the  dentin  and  imparts  an  abnormal 
color  to  a  portion  or  nearly  all  of  the  crown,  which  ranges  from 
an  almost  imperceptible  loss  of  translucency  to  a  yellow-brown, 
slate-gray,  or  bluish-black  color.  Also  in  conditions  of  venous 
hyperemia  or  pulpitis,  with  which  venous  hyperemia  (stasis)  is 
associated,  the  escape  of  the  red  corpuscles  into  the  tissue,  their 
disintegration,  and  the  solution  of  the  hemoglobin  then  occurs,  and 
the  solution  enters  the  tubules,  staining  the  dentin  a  pink  color, 
which  soon  passes  into  a  purplish  rose,  and  finally  becomes  bluish- 
black  or  slate-gray. 

Those  cases  resulting  in  the  yellowish  or  brownish  coloration  are 
usually  associated  with  the  loss  of  the  pulp  in  comparatively  sound 
or  totally  sound  teeth,  the  loss  occurring  probably  through  trauma- 
tism or  through  slow  atrophic  changes,  such  as  occur  in  the  forma- 
tion of  pulp  nodules,  secondary  dentin,  apical  constriction,  etc. 
Apical  abscess  is  often  much  delayed,  but  sometimes  occurs,  showing 
that  pulp  decomposition  or  a  later  infection  has  occurred.  The 
demonstration  by  Hopewell-Smith  of  fibrosis  of  the  pulp  and  the 
obliteration  of  vascular  structures  may  account  for  a  lessened  vas- 
cularity, and  the  absence  of  the  production  of  iron  sulphid  because 
of  the  absence  of  necessary  putrefaction  and  the  production  of  the 
hematoidin  products,  as  shown  below.  The  first  class  of  cases  occurs 
either  in  sound  teeth  in  which  the  pulps  have  died  by  traumatism, 
or  in  filled  teeth  with  pulps  not  exposed,  or  in  teeth  the  pulps  of  which 
are  exposed  to  the  fluids  of  the  mouth,  permitting  putrefactive 


BLEACHING  METHODS,  581 

agencies  and  extraneous  coloring  or  color-setting  materials  to  enter. 
This  discoloration  is  most  rapid  in  the  exposed  cases. 

These  color  changes  are  rationally  explained  by  Kirk^  as  due  to 
the  decomposition  products  of  hemoglobin  existing  in  the  pulp  at 
the  time  of  its  death,  and  having  an  analogue  in  the  pigmentary 
degeneration  occurring  in  the  hemoglobin  in  a  bruise  (extravasation 
of  blood),  in  which  the  part  becomes,  first,  "black  and  blue,"  then 
passes  through  a  series  of  color  changes,  in  which  yellow,  green,  and 
bluish-black  are  notable.  These  are  due  to  new  chemical  compounds 
which  crj^stallize  in  the  tissue.  These  compounds  are  divided  into 
two  classes:  Hemosiderins,  or  those  containing  iron,  and  hema- 
toidins,  those  without  it.  Each  class  of  these  has  several  distinct 
substances  in  it,  each  having  its  own  color  molecule. 

Kirk  states  that  methemoglobin  is  brownish-red,  hemin  bluish- 
black,  hematin  dark  brown  or  bluish-black,  and  hematoidin  orange. 

Jakob  (Stengel)  gives  light  pea-green  and  brownish-red  as  the 
colors  of  hematoidin  for  an  old  hemorrhagic  focus,  showing  a  prob- 
able slight  chemical  variation  in  the  composition  of  the  color  molecule. 

As  the  color  changes  in  a  bruise  are  effected  under  aseptic  con- 
ditions, and  usually  the  colors  finally  produced  are  lighter  than 
the  "black  and  blue"  first  resulting,  it  is  rational  to  suppose  that 
the  yellowish  or  brownish  discoloration  of  teeth  results  under  such 
conditions  of  aseptic  decomposition  (probably  autolysis).  These 
colors,  as  remarked  by  Kirk,  are  more  or  less  permanent. 

When  a  permanent  or  progressively  darkening  slate-gray  or 
bluish-black  color  is  produced,  it  is  considered  by  Kirk  to  be  due  to 
the  formation  of  iron  sulphid  or  an  analogous  product  in  which  iron 
and  sulphur  are  constituents,  and  that  it  is  analogous  to  the  black 
discoloration  occurring  in  the  visceral  walls  of  animals  undergoing 
putrefactive  decomposition.  The  iron  is  liberated  from  the  hemo- 
globin present  by  putrefaction,  and  combines  w^ith  the  ammonium 
sulphid  which  is  formed  from  the  ammonium  and  hydrogen  sulphid 
produced  by  the  putrefactive  decomposition. 

Treatment. — The  treatment  of  discolorations  consists  in  what  is 
known  as  the  bleaching  process,  which  means  the  reduction  of  the 
color  molecule  to  another  chemical  molecule  which  is  colorless,  and 
then  washing  that  out  of  the  tubules.  This  is  usually  done  by  the 
use  of  chemicals  which  directly  supply  a  molecule  of  nascent  oxygen 
when  coming  in  contact  with  the  putrefactive  material  or  its  product, 
the  color  molecule;  or  which,  as  chlorin,  abstract  hydrogen  from 
the  water  present  and  so  liberate  a  molecule  of  nascent  oxygen, 
which  combines  with  the  color  molecule.    These  are  direct  or  indirect 

1  American  Text-book  of  Operative  Dentistry. 


582  GANGRENE  OF  THE  PULP 

oxidizing  agents,  the  effect  being  the  same,  i.  e.,  an  oxidation  of  the 
color  molecule.  A  second  class,  as  sulphurous  acid,  which  abstract 
oxygen  from  the  color  molecule,  are  called  reducing  agents,  and  may 
be  effective  when  the  oxidizing  agents  fail. 

In  the  use  of  bleaching  agents  the  canal  should  have  been  cleansed 
and  disinfected  with  a  simple  aqueous  solution  of  formalin  or  25  per 
cent,  ethereal  pyrozone,  or  an  aqueous  solution  of  hydrogen  dioxid, 
or  with  sodium  dioxid,  all  oils  or,  other  materials  likely  to  complicate 
the  color  molecule  being  avoided.  With  the  exception  of  formalin, 
these  are  also  bleaching  agents  and  to  an  extent  aid  the  subsequent 
operation.  Formalin  would  best  be  avoided  in  cases  of  recent  pulp 
death,  as  it  may  harden  the  undecomposed  fibrils  in  the  dentin.  The 
upper  half  or  two-thirds  of  the  canal  should  then  be  filled  with  gutta- 
percha or  oxychlorid  of  zinc,  leaving  the  crown  and  one-third  of  the 
root  dentin  to  be  bleached. 

After  accurate  rubber  damming  the  most  valuable  and  facile 
method  consists  of  placing  a  pellet  of  cotton  saturated  with  25  per 
cent,  ethereal  pyrozone  in  the  pulp  chamber  and  sealing  it  after 
careful  drying  of  the  lingual  tap  or  cavity  orifice  by  dropping  soft, 
quick-setting  cement  upon  the  margin  and  sealing  the  entire  tap. 

The  rubber  dam  should  not  be  removed  until  the  cement  has  set, 
as  the  ether  or  oxygen  gas  may  cause  it  to  bulge  or  blister.  This  is 
then  allowed  to  have  twenty-four  or  even  more  hours  of  action,  when, 
if  necessary,  it  may  be  removed.  The  operation  may  be  watched  at 
the  first  or  the  second  sitting  if  desired,  though  it  may  be  somewhat 
prolonged. 

Aqueous  25  per  cent,  pyrozone  may  be  made  by  shaking  together 
in  a  test-tube  one  volume  of  distilled  water  and  two  volumes  of 
25  per  cent,  ethereal  pyrozone  and  evaporating  the  ether,  the  H2O2 
being  left  in  aqueous  solution;  the  addition  of  sodium  acetate  or 
sulphate  assists  the  passage  of  the  current.  This  is  introduced  by 
means  of  the  cataphoric  current,  the  positive  pole  being  in  the  tooth, 
the  negative  at  the  hand.  Occasionally  the  reversal  of  the  pole 
succeeds  after  failure,  the  tubular  contents  probably  being  discharged 
with  the  H2O2  present  in  them. 

Oxygen  may  be  liberated  from  sodium  dioxid  (Na202)  by  sulphuric 
acid.  A  saturated  solution  of  sodium  dioxid  is  made  by  surrounding 
a  small  beaker  containing  about  2  drams  of  distilled  water,  with 
cracked  ice.  When  cold  the  sodium  dioxid  powder  is  to  be  slowly 
dusted  into  it  until  it  assumes  a  semi-opaque  appearance,  indicating 
saturation.  In  use  the  dried  dentin  is  saturated  with  it,  asbestos 
fibre  being  used  to  carry  it  to  place,  and  10  per  cent,  sulphuric  acid  is 
used  to  produce  the  liberation  of  oxygen  with  the  following  equation : 
Na202  +  H2SO4  =  Na2S04  +  H2O2. 


BLEACHING  METHODS  .  583 

The  effervescence  forces  the  tubular  contents  out.  The  sodium 
dioxid  acts  upon  putrefactive  material,  decomposing  it,  and  also 
saponifies  fatty  matters. 

If  the  operation  fall  short  of  success,  this  is  due,  in  Kirk's  opinion, 
to  the  formation  of  iron  oxid,  which  can  be  removed  with  oxalic  acid 
by  sealing  a  crystal  of  it  in  the  pulp  chamber  for  twenty-four  hours. 

The  tubular  contents  being  entirely  removed  by  the  sodium-dioxid 
method,  the  tooth  is  more  translucent  than  by  other  bleaching 
methods  in  which  the  bleached  organic  debris  remains  in  the  tubules. 

The  chlorin  method,  introduced  by  Truman,  depends  for  its 
efficiency  upon  the  affinity  of  chlorin  for  hydrogen,  forming  hydro- 
chloric acid  (HCl).  Finding  this  in  the  water,  it  liberates  nascent  O, 
which  oxidizes  the  color  molecule,  or,  possibly,  it  abstracts  H  from 
the  organic  matter.  The  chlorin  is  usually  evolved  from  chlorinated 
lime,  that  sold  in  paraffined  paper  cartons  or  glass  bottles  being  the 
best.  That  sold  in  metal  cans  is  often  contaniinated  by  the  metallic 
chlorids. 

The  dry  powder  is  packed  into  the  cavity,  moistened  with  50  per 
cent,  acetic  acid,  and  sealed  in  with  oxyphosphate  or  temporary 
stopping  for  one  or  two  days,  and  repeated  if  necessary.  Only  vul- 
canite, bone,  ivory,  or  wood  instruments  should  be  used,  as  metal 
instruments  are  acted  upon  by  the  chlorin.  All  gold  or  metallic 
fillings  should  be  removed  for  the  same  reason,  and  if  their  removal 
would  cause  hardship  or  so  render  the  tooth  into  a  condition  indi- 
cating crowning,  either  this  should  be  done  or  the  direct  oxidizing 
method  tried. 

The  liberation  of  sulphurous  acid  may  be  induced  from  a  powder 
consisting  of  a  mixture  of  sodium  sulphite,  100  grains,  and  boric 
acid,  70  grains,  separately  desiccated  and  afterward  ground  together 
in  a  mortar,  by  acting  upon  it  with  a  drop  of  water.  The  cavity  is 
stopped  by  a  plug  of  gutta-percha  previously  prepared  and  warmed. 
The  following  reaction  occurs : 

2H3BO3  +  SNaoSOs  =  2Na3B03  +  SHaO  +  3SO2. 

In  all  the  methods,  except  the  use  of  Na202,  the  apex  of  the  canals 
should  be  sealed  before  and  after  bleaching;  at  least  1  pint  of  hot 
distilled  water  should  be  forcibly  injected  into  the  tooth  to  dissolve 
out  all  products  of  chemical  action  remaining  in  the  tubules,  a  towel 
being  used  to  catch  the  drip.  The  tooth  is  then  thoroughly  dried, 
and  if  any  organic  matter  may  be  present  in  the  tubules  the  pulp 
cavity  should  be  thinly  lined  with  oxychlorid  of  zinc  to  coagulate 
it.  If  it  has  been  removed,  as  in  the  sodium  dioxid  method,  leaving 
the  tubules  empty,  they  should  be  filled  with  cavitin  varnish  after 


584  GANGRENE  OF  THE  PULP 

desiccation  to  promote  absorption,  and  the  thin  lining  then  placed. 
A  temporary  filling  is  to  be  inserted  over  this  until  success  is  evident, 
when  the  permanent  work  is  completed  with  zinc  phosphate  and  a 
metal  filling. 

The  removal  of  metallic  stains  has  been  referred  to  on  page  335. 

Moist  Gangrene  of  Pulps  of  Temporary  Teeth. — The  same  con- 
siderations pertain  to  moist  gangrene  of  the  pulps  of  temporary 
teeth,  but  as  the  roots  are  resorbed  to  some  extent  or  are  to  be 
resorbed,  the  root  filling  should  be  of  such  a  character  as  to  permit 
its  resorption.  Probably  a  combination  of  paraffin  and  aristol  will 
best  fulfil  the  indications.  An  iodoform  paste  is  preferred  by  some. 
(See  Root  Canal  Filhngs.) 

If  the  roots  be  much  resorbed,  it  is  better  to  use  a  material  which 
will  permit  venting  of  the  tooth  if  necessary.  The  canals  and  pulp 
chamber  may  be  filled  with  a  combination  of  vaselin  and  aristol,  and 
this  covered  by  a  filling.  If  trouble  arise,  a  spear  drill  is  driven  into 
the  pulp  cavity  from  a  point  beneath  the  gum  margin,  establishing 
a  vent.  The  patient  should  be  instructed  to  keep  this  open,  and  be 
furnished  a  Swiss  broach  for  the  purpose. 

At  an  age  when  the  permanent  tooth  will  shortly  thereafter  erupt, 
extraction  of  the  temporary  tooth  is  often  to  be  preferred  to  treat- 
ment. 

Root-canal  Work  in  Cases  of  Gangrenous  Pulps  Involving  Future 
Consideration. — In  some  cases  of  doubtful  root  sterilization  or  filling, 
and  in  which  crowning  by  means  of  dowelled  crowns  is  a  necessity, 
provision  may  be  made  for  future  relief  or  treatment  by  the  employ- 
ment of  one  of  two  excellent  methods  of  procedure : 

1.  Kirk  has  suggested  that  the  post  and  band  of  a  Richmond  crown 
be  painted  while  warm  with  a  solution  of  gutta-percha  in  chloroform. 
The  solvent  evaporates,  leaving  a  coating  of  gutta-percha.  This 
should  be  reasonably  thick.  The  crown  is  then  set  with  cement. 
By  warming  the  crown  with  a  hot  crown-setting  tool  (How)  or 
forceps,  it  may  be  removed  without  destruction  of  the  piece. 
Bridges  so  set  are  very  firm.  The  crown  may  be  set  with  gutta- 
percha alone  or  in  some  cases  with  temporary  stopping. 

2.  Gird  wood  (Edinburgh)  has  suggested  root  intubation,  the  tube 
being  closed  at  the  end  with  temporary  stopping  and  then  set  with 
cement.  Immediately  thereafter  the  temporary  stopping  and  soft 
cement  are  removed  with  Donaldson  cleansers,  leaving  the  root 
lumen  free  to  the  apical  foramen  or  root  filling.  The  tube  and  canal 
are  then  treated  as  a  continuous  root  canal  would  be.  The  idea  is 
also  applied  to  a  Richmond  or  all-porcelain  crown,  the  tube  being 
used  in  place  of  the  pin,  and  allowed  to  extend  through  the  backing, 
to  be  later  filled  as  desired. 


SECTION  Y. 

DISEASES  OF  THE  PERICEMENTUM. 


CHAPTER  XIX. 
SEPTIC  APICAL  PERICEMENTITIS  (ACUTE). 

Classification  — The  dental  periosteum  and  ligament,  or  the  peri- 
cementum, is  the  seat  of  numerous  nutritive  and  functional  disturb- 
ances, which  may  be  grouped,  according  to  their  causes,  into  septic 
and  non-septic. 

The  term  pericementitis  has  been  indiscriminately  applied  to  all 
affections  of  the  pericementum,  and  in  some  cases  erroneously,  for  in 
not  all  affections  of  this  structure  do  the  phenomena  of  inflammation 
appear;  in  some  hyperemia  alone  may  exist.  However,  most  of  the 
acute  and  chronic  degenerations  are  accompanied  by  evidences  of 
inflammation. 

Bodecker's  division  of  the  affections  of  the  pericementum  into 
purulent  and  non-purulent  is  misleading.  Cases  may  be  due  to 
septic  causes  without  pus  formation;  pus  formation  represents  but 
one  form  of  sepsis. 

The  most  convenient  clinical  classification  of  these  disorders  is  that 
offered  by  G.  V.  Black  i^  (1)  Diseases  of  the  pericementum  beginning 
at  the  apex  of  the  root;  (2)  those  beginning  at  the  gum  margin;  (3) 
those  beginning  in  some  intermediate  portion  of  the  pericementum. 
These  may  again  be  divided,  according  to  their  causes,  into  septic 
and  non-septic.  Another  clinical  classification  would  be  into  localized 
and  general  disturbances — another  into  acute  and  chronic. 

Evidences  of "  Pericemental  Disturbance  — It  was  noted  in  the 
study  of  the  diseases  of  the  dental  pulp  that  the  diagnostic  signs  of 
pulp  disturbance  were  exaggerated  or  diminished  response  to  thermal 
stimuli;  reflected  instead  of  localized  pains;  and,  except  in  rare  cases 
of  advanced  hyperemia,  no  tenderness  upon  percussion.  Disturb- 
ances of  the  pericementum  are  accompanied  by  entirely  different 
symptoms  which  serve  to  distinguish  between  them  and  diseases  of 

1  American  System  of  Dentistry,  vol.  i. 

(585) 


586  SEPTIC  APICAL  PERICEMENTITIS 

the  pulp.  They  are,  in  general,  tenderness  upon  percussion.  As 
shown  by  Black,^  the  pericementum  is  the  touch  organ  of  the  tooth, 
its  tactile  organ,  through  which  a  tooth  locates  force  applied  to  the 
tooth.  The  pains  of  pericemental  disturbance  are,  therefore,  in  the 
majority  of  cases,  exactly  localized,  instead  of  not  being  localized, 
as  in  the  case  of  the  pulp.  A  tooth  tender  upon  percussion  has 
its  pericementum  as  the  seat  of  disturbance.  Most  cases  of  peri- 
cemental diseases  are  accompanied  by  vascular  reactions  ranging 
from  an  increased  blood  flow,  or  grades  of  hyperemia  to  pronounced 
inflammation,  and  have  the  corresponding  symptoms.  The  increased 
volume  of  the  pericementum  causes  the  protrusion  and  loosening  of 
the  tooth,  heightened  sensitivity  being  the  accompaniment.  As  the 
vascular  supply  of  the  pericementum  and  that  of  the  gum  are  in  a 
degree  collateral  (see  p.  190),  evidences  of  vascular  engorgement 
are  seen  in  the  gum  overlying  the  affected  tooth.  Owing  to  the 
altered  density  of  the  parts  surrounding  the  tooth  root,  percussion 
upon  the  tooth  elicits  a  different  sound  from  that  observed  in  health 
— the  sound  is  dull.  The  general  symptoms  of  pericemental  affections 
are,  therefore,  tenderness  upon  percussion  and  a  dull  percussion  note, 
more  or  less  protrusion,  and  looseness  of  the  tooth  and  a  deepening 
of  the  local  gum  color. 

DISEASE   OF  THE  PERICEMENTUM  BEGINNING  AT  THE  APEX. 

Diseases  of  the  pericementum  beginning  at  the  apex  of  the  root 
are  of  two  classes,  septic  and  non-septic.  The  septic  cases  are  almost 
invariably  the  sequel  to  diseases  of  the  pulp,  namely,  suppuration 
and  gangrene,  or  arise  in  consequence  of  infection  through  the  canals 
of  pulpless  teeth.  The  non-septic  cases  are  due  to  mechanical  and 
chemical  irritants,  and  in  rare  cases  to  undiscovered  causes. 

Acute  Septic  Apical  Pericementitis ;  Acute  Alveolodental  Abscess ; 
Dento-alveolar  Abscess. — Definition. — By  septic  apical  pericementitis 
is  meant  an  inflammation  of  the  apical  pericementum  due  to  the 
entrance  of  bacteria  into  the  tissue  lying  in  the  apical  space. 

Causes. — The  most  common  causes  of  septic  apical  pericementitis 
are: 

1.  Bacteria  engaged  in  the  putrefaction  of  a  gangrenous  pulp. 
The  gases  and  toxic  products  evolved  by  the  process  also  cause 
much  irritation. 

2.  Pyogenic  organisms  engaged  in  the  production  of  suppuration 
of  the  pulp  in  its  later  stages. 

1  American  System  of  Dentistry,  vol.  i. 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     587 

3.  Pyogenic  organisms  introduced  into  the  otherwise  aseptic  tissues 
of  the  apical  space  by  means  of  instrumentation  or  other  lack  of 
aseptic  precautions. 

Fig.  534 


Alveolar  abscess  pointing  externally.      The  abscess  is  caused  by  the  only-slightly- 
impacted  and  not-malposed  lower,  third  molar.      (Raper). 


4.  Infection  of  an  apical  space  by  an  abscess  arising  in  some  con- 
tiguous part  and  extending  in  the  direction  of  the  apical  space  under 
consideration. 

5.  Septic  infection  from  a  pyorrhea  pocket  located  upon  the  side 
of  the  tooth  in  question,  the  deepest  portion  of  which  approximates 


SEPTIC  APICAL  PERICEMENTITIS 

the  apical  space.  An  alveolar  abscess  about  an  impacted  tooth 
may  find  its  way  apically  and  even  discharge  through  the  cheek. 

6.  Possible  infection  by  way  of  the  pericemental  tract  from  the 
gum  margin  or  by  way  of  the  circulation,  which  infection  may  cause 
a  pericemental  abscess  located  in  the  apical  tissue. 

The  last  two  conditions  would  be  septic  apical  pericementitis, 
but  are  to  be  considered  separately  as  pericemental  abscess  or  true 
alveolar  abscess.  (See  Pyorrhea  Alveolaris.)  As  a  cause  of  apical 
abscess  it  is  rare,  but  has  been  seen. 

Apart  from  these  causes  infective  inflammation  of  apical  tissue 
does  not  seem  to  occur.  It  is  to  be  remembered  that  a  small  portion 
of  gangrenous  pulp  beneath  a  root-canal  filling  is  equivalent  to  an 
entire  gangrenous  pulp  as  a  cause  of  pericementitis.  The  vast 
majority  of  cases  occur  as  a  sequel  to  moist  gangrene  of  the  pulp, 
either  before  or  after  instrumentation,  or  as  a  result  of  infection  of 
the  apical  tissue  by  instruments  either  unsterilized  or  reinfected  by 
contact  with  the  oral  fluids. 

The  organisms  found  in  acute  apical  abscesses  are  those  usually 
found  in  gangrenous  and  suppurating  pulps,  and  in  a  certain  per- 
centage of  even  healthy  mouths.  (See  p.  51.)  Schreier  found  the 
Diplococcus  pneumoniae  in  15  out  of  20  cases  examined.  He  also 
found  Staphylococcus  pyogenes  albus  and  aureus,  and  occasionally 
Streptococcus  pyogenes. 

Arkovy  found  the  Bacillus  gangrense  pulpse  in  a  number  of  cases. 
(See  p.  568.)  These  are  virtually  the  same  organisms  that  are  found 
in  the  deeper  portions  of  a  suppurating  or  gangrenous  pulp;  this 
fact  in  itself  is  enough  to  show  the  continuity  of  infection  from  the 
pulp  canal.  It  is  a  well-known  clinical  fact  that  acute  outbreaks  of 
septic  apical  pericementitis  are  most  liable  to  occur  under  those 
conditions  when  patients  "take  cold."  Schreier  points  out  that 
these  atmospheric  states  produce  a  bodily  condition  which  favors 
the  development  of  the  Diplococcus  pneumoniae  (Pneumococcus), 
and  finds  in  the  association  of  these  factors  the  reason  why  this 
diplococcus  should  be  pathogenic  in  the  dental  condition. 

Pathology,  Morbid  Anatomy,  and  Symptoms. — The  Inflammatory 
Stage. — As  in  abscess  elsewhere  there  is  first  infection  by  pyogenic 
organisms  wliich  produce  the  phenomena  of  infective  inflammation 
within  the  substance  of  the  apical  tissue,  and  in  the  later  stages  in 
the  contiguous  tissues. 

Following  the  infection,  arterial  hyperemia  is  produced,  sensation 
is  exalted,  and  the  tooth  becomes  tender  upon  percussion;  but  if 
forcibly  pressed  upon — ?".  e.,  if  the  arteries  be  compressed — the 
hyperemia  is  momentarily  lessened  and  the  pressure  brings  a  sense 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     589 

of  relief.     At  this  stage  the  gum  over  the  apex  looks  normal,  but 
may  respond  to  pressure. 

Following  the  arterial  hyperemia,  the  venous  obstruction  which 
ends  in  stasis  is  inaugurated  and  diapedesis  of  leukocytes  and  fibrin- 
ous exudation  into  the  intervascular  tissue  occurs.  The  fixed  cells 
undergo  proliferation. 

Fig.  535 


.s 


Showing  the  morbid  anatomy  of  septic  apical  pericementitis  (acute):  A,  pus;  B, 
area  of  dying  leukocytes;  C,  septic  matter  in  root  canal;  D,  inflammation  of  process 
(osteomyelitis;  area  of  lesser  inflammation);  E,  swollen  periosteum  and  gum,  hyper- 
emic;  F,  alveolar  bone  in  a  stage  of  hyperemia;  G,  pericementum  at  edge  of  necrosis. 


As  this  condition  of  inflammation  becomes  established  the  pain  due 
to  pressure  upon  the  sensory  nerves  becomes  of  a  violent  throbbing 
character,  accompanied  by  a  sense  of  fulness.  The  swelling  of  the 
tissue  about  the  apex  of  the  root,  due  to  the  excess  of  fluid,  blood, 
leukocytes,  and  tissue  cells,  of  necessity  pushes  the  tooth  from  its 
socket,  so  that  it  feels  and  is  longer  than  the  other  teeth.  Moreover, 
as  it  is  bitten  upon  the  apical  tissue  is  further  irritated.  The  tooth  is 
loosened  and  percussion  induces  pain  and  elicits  the  dull  note  which 
is  diagnostic  of  the  increase  of  bulk  in  the  pericementum.  The  color 
of  the  gum  over  the  root  becomes  deepened. 

First  Stage  of  Pus  Formation. — The  central  area  of  the  apical 
tissue — i.  e.,  that  next  the  apical  foramen — is  broken  down  into  pus, 
some  of  which  enters  the  root  canal  (Fig.  535,  A).  As  the  area  of 
pus  formation  widens,  all  of  the  apical  tissue  is  liquefied  (Fig.  538,  a). 


590 


SEPTIC  APICAL  PERICEMENTITIS 


From  a  clinical  point  of  view  the  abscess  is  incipient  when  inflamma- 
tion of  the  apical  tissue  next  to  the  foramen  is  profound,  and  pus 


Fig.  536 


Fig.  537 


A  cyst  extending  from  left  lower  second   bicuspid   to 
the  central  of  same  side.      The  central  has  a  root  filling. 
Method   of    accurately  de-       In  absence  of  other  things  this  may  be  regarded  as  the 
termining  length  of  root.  origin  of  the  cyst. 


Fig.  538 


Acute  abscess  in  second  stage.     Tooth  opened  at  h  for  treatment,  making  an  abscess, 
discharging  via  the  canal.     (Black.) 


Fig.   539 


Fig.  540 


Abscess  on  crowned  root.     (Skiagraph 
by  Lodge.) 


Abscess  on  incomplete  root.      (Skis 
graph  by  Lodge.) 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     591 


Fig.  541 


formation  has  just  begun  (Fig.  535).    The  first  stage  continues  while 
the  pus  is  in  the  apical  tissue. 

Second  Stage  of  Pus  Formation. — The  bone  cells  become 
involved  in  the  process  and  are  destroyed  (osteitis).  The  throbbing 
pain,  the  extrusion,  looseness,  and  dulness  to  percussion,  and  the 
inflammation  and  edema  of  the  contiguous  tissues  are  marked.  The 
gum  is  widely  inflamed,  reddened,  and  swollen,  but  no  demarcation 
of  an  abscess  may  be  noted  upon  the  gum  at  this  stage.  The  mem- 
branes of  the  adjoining  teeth  become  irritated  and  hyperemic,  and 
they  may  exhibit  tenderness  upon  percussion  (Fig.  538). 

Third  Stage  of  Pus  Formation. — The  pus  continues  to  form 
in  all  directions  until  the  bone  is  perforated  at  some  point — i.  e., 
usually  through  the  labial  alveolar  plate  —  that  being  the  thin- 
nest and  most  readily  per- 
forated. The  periosteum  is 
now  destroyed  and  the  gum 
tissue  directly  involved  as  a 
boundary  to  the  pus,  which 
collecting  beneath  it,  raises  it 
into  a  distinctly  demarked 
tumefaction  (Fig.  541,  6).  The 
pain  becomes  less  acute,  owing 
to  the  binding  resistance  of 
the  gum  being  less  than  that 
of  the  bone.  At  first  the 
swelling  is  hard,  and  this 
represents  a  mass  of  gum  tis- 
sue overlying  pus;  later,  it 
softens  at  its  highest  point, 
pus  appears  as  a  yellow  spot 
beneath  the  mucous  mem- 
brane. The  mucous  mem- 
brane bursts  and  a  discharge 
of  pus  follows.  The  inflam- 
mation and  tenderness  then 
largely  subside,  but  some  de- 
gree of  looseness  and  protru- 
sion remains. 

During  the  latter  part  of  the  second  and  in  the  third  stage  of  pus 
formation,  instead  of  the  swelling  extending  but  little  beyond  the 
overlying  gum,  the  tissues  of  the  lips,  cheeks,  or  neck  may  be  very 
much  swollen  and  with  upper  teeth  the  eye  of  the  affected  side 
injected.    In  some  cases  the  outer  skin  may  become  reddened  and 


Acute  alveolar  abscess  of  a  lower  incisor  in 
the  third  stage,  with  pus  cavity  between  the 
bone  and  the  periosteum:  a,  pus  cavity  in 
the  bone;  b,  pus  between  the  periosteum  and 
bone;  c,  lip;  d,  tooth;    e,  tongue.   (Black.) 


592  SEPTIC  APICAL  PERICEMENTITIS 

dusky,  exhibiting  the  evidences  of  extension  of  the  inflammatory 
process  far  from  its  original  site. 

The  inflammatory  process  spreads  out  from  the  central  focus  of 
pus  formation,  there  being  around  the  pus  a  zone  of  active  inflamma- 
tion or  stasis;  about  this  one  of  a  lesser  degree  of  inflammation,  also 
full  of  leukocytes;  about  this  an  area  of  arterial  hyperemia  or  the 
first  stage  of  inflammation,  and  around  this  normal  tissue.  These 
areas  are  not  sharply  defined,  but  merge  into  one  another  (Fig.  535, 
A,  D,  E,  F;  also  p.  135  and  Fig.  64). 

In  this  way  the  contiguous  area  of  the  alveolar  bone  and  the  soft 
tissues  of  the  face  become  involved  in  the  process,  being  discolored 
and  tumefied  in  proportion  to  the  extent  of  the  pus  formation  and 
the  inflammatory  reaction  thereto. 

While  in  the  vast  majority  of  cases  the  direction  taken  by  the  pus, 
and  the  point  at  which  it  flnds  exit,  is  the  buccal  or  labial  aspect,  and 
immediately  over  the  root  apex  of  the  affected  tooth,  or  near"  it, 
these  being  the  directions  of  least  resistance,  other  anatomical  con- 
ditions or  histological  peculiarities  may  make  the  direction  of  least 
resistance  in  some  other  path  (Figs.  542  to  545). 

Instead  of  the  circumscribed  suppuration  described  as  the  ordinary 
course  of  abscess  formation  about  the  apices  of  roots  (septic  apical 
pericementitis)  which  accompanies  infection  by  the  staphylococci, 
clinical  evidences  of  infection  by  streptococci  occasionally  appear. 
The  inflammatory  process,  instead  of  being  circumscribed,  is  diffuse; 
the  inflammation  extends  along  the  lines  of  the  connective  tissues 
and  of  the  lymphatics;  the  connective  tissues  are  swollen,  the  swelling 
extending  to  the  tissues  of  the  cheek,  down  the  neck,  and  even  to 
the  shoulder — a  phlegmonous  inflammation.  Instead  of  the  com- 
paratively free  flow  of  pus  which  follows  incision  of  the  swelling  in 
ordinary  abscess,  pus  formation  in  streptococcus  infection  is  seen, 
upon  incision,  to  be  limited  and  seropurulent.  While  in  alveolar 
abscess  of  the  ordinary  types  evidences  of  septic  intoxication  or 
poisoning  are  unusual,  the  lymphatics  being  blocked,  as  a  rule,  by 
the  inflammatory  exudates,  septic  intoxication  and  poisoning  are  the 
rule  in  the  erysipelatous  cases,  those  probably  due  to  streptococcus 
infection;  bacterial  poisons  being  taken  up  by  the  lymphatics  find 
their  way  into  the  circulation. 

The  symptoms  of  the  absorption  of  bacterial  products  from  the 
circumscribed  abscesses  are:  Fever,  often  ushered  in  by  a  distinct 
chill.  The  pulse  increases  in  volume  and  tension;  it  is  full,  hard, 
and  frequent.  The  tongue  is  coated,  the  bowels  constipated.  The 
patient  is  also  weakened  and  made  irritable  by  pain  and  attendant 
loss  of  sleep  and  appetite. 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX      593 

In  the  streptococcal  infection  there  is  danger  that  these  may 
change  into  the  more  profound  symptoms  of  septicemia — i.  e.,  a 
soft,  frequent  pulse,  repeated  chills,  diarrhea,  clammy  skin,  general 
depression,  and  a  disordered  nervous  system. 

In  multirooted  teeth  the  inflammation  and  abscess  frequently 
appear  on  only  one  root.  If  the  case  be  seen  early,  before  the  active 
exudation  period  of  the  inflammation  sets  in,  the  symptoms  may  be 
clearly  localized  in  one  root,  the  tooth  exhibiting  tenderness  upon 
pressure  over  the  affected  root,  but  not  upon  the  opposite  side. 

After  spontaneous  discharge  of  the  pus  from  an  abscess,  the 
condition  remaining  is  that  of  an  ulcerous  surface  (the  abscess 
boundaries)  which  is  being  continuously  infected  from  the  putrescent 
pulp  remnants.  The  conditions,  it  is  seen,  are  not  like  those  of 
ordinary  abscess,  where  the  infective  material  is  largely  discharged 
in  the  pus  evacuation,  and  the  cells  bounding  the  abscess  wall 
dispose  of  remaining  bacteria,  so  that  regeneration  of  tissue  occurs. 
Spontaneous  healing  of  an  apical  abscess  is  the  exception;  the 
embryonic  tissue  lining  the  abscess  walls,  being  continuously  infected, 
degenerates  and  dies  as  fast  as  it  forms,  leaving  a  condition  known 
as  chronic  apical  abscess,  or  chronic  purulent,  apical,  septic  peri- 
cementitis. 

Clinical  History. — The  clinical  history  of  acute  alveolar  abscess 
may  be  divided  into  three  stages:  (1)  That  of  initial  inflammation 
and  pus  formation;  (2)  the  destruction  of  the  alveolar  process;  (3) 
the  passage  of  pus  through  the  periosteum  and  mucous  membrane. 
The  second  stage  is  usually  the  longest.  The  duration  of  the  disease 
depends  upon  the  readiness  with  which  the  tissues  between  the  point 
of  beginning  pus  formation  and  its  exit  yield.  When  the  pulp 
chamber  is  open  pus  may  find  exit  by  this  path,  constituting  the 
condition  known  as  blind  abscess — a  misnomer,  because  a  blind 
abscess  is  one  without  a  point  of  discharge,  without  a  fistula  leading 
to  it;  in  the  cases  discharging  via  the  canal,  the  latter  may  be 
considered  a  fistula  (Fig.  538). 

Acute  abscesses  usually  run  a  short  course,  the  inflammatory 
symptoms  being  severe  and  the  tissue  destruction  limited.  Notably 
upon  lower  molars,  and  upon  the  lingual  roots  of  upper  molars, 
the  density  and  thickness  of  bone  overlying  the  roots  may  make 
paths  of  greatly  increased  resistance,  so  that  the  destruction  of 
tissue  proceeds  along  the  line  of  the  pericementum,  the  pus  finding 
exit  at  the  neck  of  the  tooth.  It  is  rare  in  cases  of  lower  second 
molars,  and  still  more  rare  upon  the  third  molars,  that  pus  finds 
exit  over  the  apex  of  the  root,  the  dense  botie  of  the  external  oblique 
line  offering  the  greatest  resistance  (Fig.  542).  Over  any  teeth 
38 


594 


SEPTIC  APICAL  PERICEMENTITIS 


the  outer  fibrous  layers  of  the  external  periosteum  may  present 
unusual  resistance  to  the  perforative  advance  of  pus,  so  that  when 
the  fibers  of  attachment  of  the  periosteum  have  been  softened  by 
the  inflammation,  and  pus  gains  entrance  between  bone  and  peri- 
osteum, it  may  travel  or  burrow  along  the  course  of  this  membrane 
(Fig.  543),  depriving  the  bone  of  its  main  nutritive  source,  so  that 
limited  necrosis  threatens.  The  roots  of  the  central  incisors  may  lie 
unusually  close  to  the  floor  of  the  nose,  and  be  overlaid  externally 
by  an  unusually  resistant  layer  of  bone;  in  these  cases  the  path  of 
least  resistance  may  be  in  the  direction  of  the  floor  of  the  nose,  the 
abscess  opening  at  that  point  (Fig.  544),  or  the  pus  may  perforate 
the  lingual  alveolar  plate,  and,  raising  the  periosteum  and  mucous 
membrane,  form  a  large  swelling  upon  one  side  of  the  hard  palate. 


Fig.  542 


Fig.  543 


Abscess  upon  lower  third  molar, 
showing  the  usual  paths  of  pus  exit,  A 
and  B. 


Abscess  upon  palatal  root  of  an  upper  molar 
discharging  at  the  neck  of  the  tooth. 


Vederspiel^  instances  a  case  in  which  an  abscess  starting  upon 
an  upper  third  molar  finally  infected  the  tonsil  producing  an  abscess, 
also  produced  necrosis  of  a  portion  of  the  ramus  of  the  inferior 
maxilla. 

The  root  apices  of  the  posterior  upper  teeth,  particularly  of  the 
first  and  second  molars,  may,  after  the  age  of  twenty-five  or  thirty, 
be  encroached  upon  by  the  enlarging  maxillary  sinus,  so  that  any 
or  all  of  the  roots  of  these  teeth  may  be  separated  from  the  floor  of 
the  sinus  by  but  a  very  thin  lamina  of  bone  or  only  by  periosteum 
and  mucosa;  should  abscess  arise  upon  any  of  these  roots,  pus 
discharge  into  the  antrum  would  necessarily  follow.  In  these  cases 
the  acute  symptoms  may  rapidly  subside,  but  later  symptoms  of 
antral  empyema  may  follow  (Fig.  545). 


1  Dental  Cosmos,  December,  1912. 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     595 

Resort  to  the  use  of  poultices  upon  the  face,  for  the  rehef  of  the 
pain  of  abscess  formation,  may  induce  such  a  softening  of  the  tissue 
over  which  they  are  appHed  that  the  passage  of  pus  is  invited  toward 
the  exterior;  the  abscess  may  thus  open  upon  the  face  or  neck, 
producing  permanent,  disfiguring  scars  (Fig.  583). 


'^'^$^sy 


Alveolar  abscess  at  the  root  of  a 
superior  incisor,  discharging  into 
the  nose:  a,  large  abscess  cavity  in 
the  bone;  b,  mouth  of  fistula  on 
the  floor  of  nostril;  c,  lip;  d.  tooth. 
(Black.) 


Alveolar  abscess  at  the  root  of  an  upper 
molar  discharging  into  the  antrum  of  High- 
more:  a,  abscess  cavity  in  the  bone;  b, 
mouth  of  fistula  on  the  floor  of  the  antrum; 
c,  pus  in  the  antral  cavity.     (Black.) 


In  patients  who  are  in  a  cachectic  condition,  who  have  an  evil 
heredity,  or  whose  tissue  resistance  is  markedly  lessened  in  conse- 
quence of  tuberculosis, .  or  more  frequently  of  syphilis,  septic  peri- 
cementitis may  run  a  riotous  course;  the  bone  suffers  extensively  by 
direct  action;  the  periosteum  is  undermined,  is  stripped  from  the 
bone  over  large  areas,  and  breaks  down  readily;  so  that  while  in 
the  healthy  person  alveolar  abscess  formation  may  run  a  direct 
course  and  find  prompt  outlet,  in  the  syphilitic  patient  extensive 
pus  infiltration,  with  necrosis,  may  occur.  In  cachectic  persons  lym- 
phatic involvement  is  common;  waste  products  of  bacterial  origin 
find  their  way  into  the  lymphatics,  and  set  up  secondary  irritative 
processes  in  the  nearest  lymphatic  glands — lymphadenitis. 

In  persons  whose  oral  hygiene  is  neglected  the  third  stage  of 
alveolar  abscess  is  frequently  violent  and  the  inflammatory  process 
widespread. 

Diagnosis. — In  incipient  apical  pericementitis  the  symptoms  may 
consist  of  reflex  pains,  but,  as  a  rule,  are  distinctly  localized  in  the 
teeth  affected,  which  are  tender  to  the  touch.  The  discoloration  of 
the  tooth  crown  and  other  evidences  of  moist  gangrene  are  usually 
present  unless  the  tooth  has  been  previously  partially  treated,  when 


596 


SEPTIC  APICAL  PERICEMENTITIS 


the  color  may  be  good,  but  by  transmitted  light  opacity  is  noted 
In  a  few  cases  the  tooth  has  had  almost  a  normal  color  even  under 
the  transmitted  light.    In  the  pronounced  cases  the  symptoms  are  as 
described  (see  p.  570). 

When  a  sinus  is  present  a  soft  silver  probe  may  often  be  passed 
toward  the  tooth  affected. 

A  timid  patient  will  often  unintentionally  confuse  pericemental 
tenderness  with  the  pain  of  sensitive  dentin. 


Fig.  546 


Fig.  547 


Diagnosis  of  apical  abscess  by 
a;-rays.   (Price. i) 


Skiagraph  of  perforation  and  apical  abscess;  wire 
thrust  through  same.     (Lodge's  method.) 


In  very  doubtful  cases,  as  when  molars  have  deep  amalgam  fillings, 
or  pins  have  been  placed  in  root  canals,  or  gold  crowns  cover  the 
natural  crowns,  either  the  covering  must  be  removed  or  a  skiagraph 
be  taken. 

After  high  inflammation  has  existed  for  twenty-four  hours,  pus  is 
generally  present  in  the  apical  tissue. 

Of  two  pulpless  teeth  surrounded  by  a  zone  of  inflammation,  the 
more  tender  and  loosened  is  the  one  affected,  though  both  may  be 
acting  at  once.  It  is  to  be  remembered  that  adjoining,  otherwise 
normal,  teeth  may  show  some  evidence  of  pericementitis,  due  to 
extension,  so  that  differentiation  is  necessary.  The  various  stages 
of  inflammation  and  pus  formation  are  judged  by  the  appearance  of 
the  gum  or  by  the  x-rays  (Fig.  546).  The  greater  the  swelling  and 
injection  of  the  gum,  the  more  advanced  is  the  pus  formation. 

The  inflammatory  action  precedes  the  advance  of  pus,  which 
furnishes  a  guide  to  the  direction  the  pus  is  pursuing — viz.,  where 
the  most  intense  coloration  and  the  greatest  swelling  appears  will  be 
the  point  at  which  the  abscess  will  point  or  discharge.  A  sudden 
subsidence  of  inflammation  without  an  immediately  discoverable 


I  Items  of  Interest,  1901. 


Fig.  548 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     597 

point  of  pus  exit  should  lead  to  the  suspicion  that  the  discharge  has 
taken  place  in  an  unusual  situation. 

The  direction  pus  may  take  is  often  determined  by  gravity,  but 
the  resistance  of  certain  tissues  may  cause  the  pus  to  seek  the  easiest 
path.  Thus,  by  discharging  into  the  antrum  it  goes  rather  counter 
to  gravity.  In  such  cases  as  discharge  into  the  antrum  there  is 
liable  to  be  a  collection  of  pus  in  that  cavity  which  may  cause  destruc- 
tion of  the  mucous  membrane  and  bone.  This  condition  is  known 
as  empyema  of  the  antrum.  The 
sudden  subsidence  of  an  acute  abscess 
upon  a  tooth  located  beneath  the 
antrum  should  create  a  suspicion  of 
discharge  into  that  sinus.  If  a  fine 
probe  can  be  passed  an  unusual  length 
into  a  root  canal  it  indicates  this  form 
of  sinus  involvement. 

An  abscess  originating  about  an  im- 
pacted tooth,  or  one  due  to  subperio- 
steal inflammation,  must  be  differen- 
tiated^ (Fig.  548).  A  pericemental 
abscess  must  also  be  considered.  It  is 
always  more  lateral  and  there  is  less 
facial  involvement,  also  there  is  usually 
a  pyorrhea  pocket  leading  to  it.  An 
acute  abscess  of  the  pulp  in  its  most 
pronounced  stage  may  simulate  incip- 
ient or  even  pronounced  acute  apical  pericementitis.  (See  p.  449.) 
An  abscess  sometimes  forms  beneath  the  flap  of  gum  overlying  a 
third  molar.  This  begins  as  an  ulceration  of  the  under  side  of  the 
flap,  but  the  pus  burrows  between  the  tooth  and  the  gum,  and  when 
well  confined  may  develop  laterally,  causing  the  formation  and  at 
least  partial  retention  of  a  quantity  of  pus  in  the  tissues  of  the  cheek. 
This  condition  more  nearly  simulates  the  lateral  abscess  associated 
with  a  pyorrhea  pocket,  and  as  by  extension  it  sometimes  involves 
the  tonsil,  the  case  may  be  mistaken  for  an  amygdalitis. 

The  last  three  conditions  are  usually  associated  with  suspected 
teeth  containing  vital  pulps,  so  that  tests  for  pulp  vitality  are  to  be 
applied. 

In  certain  cases  of  pulp  gangrene  part  of  the  pulp  only  may  be 
dead — e.  g.,  the  lingual  filament  of  the  pulp  of  an  upper  molar;  while 
the  balance  may  be  vital  (the  buccal  filaments) .    This  fact  may  con- 


Non-descended  cuspid  and  lat- 
eral. These  teeth  were  entirely 
enveloped  in  pus.  The  cuspid 
and  lateral  shadows  overlie  each 
other.  Between  these  and  the 
first  bicuspid  may  be  seen  three 
tiny  supernumeraries.      (Lodge.) 


1  Black:  American  System  of  Dentistry,  vol.  i. 


598  SEPTIC  APICAL  PERICEMENTITIS 

fuse  the  response  to  tests  and  is  to  be  borne  in  mind.  A  broken  root 
covered  more  or  less  by  gum  or  carious  bone  must  be  taken  into 
account. 

Prognosis.— In  the  majority  of  cases  the  prognosis  of  acute  apical 
abscess,  as  to  the  future  retention  of  the  tooth,  is  favorable;  and 
usually  very  favorable  if  the  case  receive  intelligent  therapeutic  aid. 
The  future  of  the  tooth  depends  upon  the  thoroughness  with  which 
sources  of  infection  may  be  destroyed  and  permanently  removed, 
and  the  completeness  with  which  regeneration  of  tissue  can  be  induced. 

Treatment. — In  the  initial  inflammation  and  first  stage  of  pus  for- 
mation the  treatment  should  be  abortive,  to  afford  relief  from  the 
pain.  The  cause  of  the  inflammation  should  be  removed,  if  possible, 
and  the  pus  formed  be  removed  or,  at  least,  permitted  to  escape  by 
way  of  the  pulp  canals.  The  promptness  of  relief  from  pain  depends 
upon  the  thoroughness  with  which  this  is  accomplished. 

The  pulp  chamber  should  be  opened  to  an  extent  which  perniits 
the  free  passage  of  broaches  into  the  canal  (Figs.  538  and  543). 

If  the  cavity  of  decay  be  open,  the  pulpal  wall  is  to  be  perforated. 
If  a  filling  be  present,  it  is  in  part  or  entirely  removed.  If  the  enamel 
be  entirely  sound,  or  if  subsequent  treatment  require  a  new  opening 
in  line  with  the  pulp  canals,  it  is  at  least  in  part  made. 

These  openings  are  usually  begun  with  a  small,  spear-pointed  drill 
(No.  100,  S.  S.  W.  Catalog)  revolving  in  a  perfectly  true  hand  piece. 
To  centre  the  drill,  first  spot  the  enamel  with  a  dentate  bur.  The 
opening  made  is  enlarged  with  successive  sizes  of  sharp,  round, 
dentate  burs  until  of  sufficient  size. 

According  to  the  amount  of  tenderness,  the  tooth  will  require  a 
counterpressure  to  that  of  the  drill.  If  the  entrance  be  made  through 
the  occlusal  face  of  the  tooth,  or  in  a  direction  which  would  cause 
direct  pressure  on  the  apical  pericementum,  a  ligature  of  linen 
thread  with  long  ends  may  be  placed  around  the  tooth,  and  traction 
be  made  by  drawing  on  the  loose  ends  of  the  ligature.^  Effective 
counterpressure  against  lateral  entrance  to  the  pulp  chamber  may 
be  made  by  softening  a  small  roll  of  modelling  compound  and  mould- 
ing over  the  face  of  the  affected  tooth  and  several  of  those  adjoining 
it,  and  hardening  with  cold  water.  This  temporary  splint  is  held  in 
place  by  the  index  finger  of  the  left  hand.  W.  D.  Tracy  recommends 
for  posterior  teeth  a  double  modeling  compound  splint,  one  lingual 
one  buccal,  to  be  held  with  the  fingers,  or  two  ligatures  may  be 
placed  between  the  tongue  before  the  compound  is  placed  and  the 
ends  tied  over  the  splints,  binding  them  against  the  teeth.     In  case 

1  J.  Foster  Flagg:  Lectures  on  Dental  Therapeutics. 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX      599 

the  inflammatory  process  is  marked,  or  if  the  patient  be  in  bed,  it 
may  be  necessary  to  make  a  vent  opening  by  the  easiest  path,  espe- 
cially when  using  a  hand  drill — i.  e.,  at  the  junction  of  enamel  and 
cementum — directly  into  the  chamber. 

As  soon  as  entrance  to  the  pulp  chamber  is  effected,  the  cavity 
is  syringed  with  a  strong  antiseptic.  Fine  probes  are  passed  and 
repassed  into  the  opening  to  free  the  outlet,  so  that  gases  and  pus 
may  escape  and  fresh  portions  of  the  antiseptic  be  worked  into  the 
cavity.  The  escape  of  blood  from  the  canal  is  a  sign  that  all  the  pus 
is  vented.  The  quickness  with  which  relief  is  secured  will  depend 
upon  the  thoroughness  with  which  the  canals  are  entered  and  their 
putrid  contents  given  vent.  A  tedious  class  of  cases  are  those  in 
which  a  canal  of  a  molar  is  filled  or  partially  filled.  Unless  entrance 
to  and  cleansing  of  the  canal  be  accomplished,  the  inflammation 
will  proceed  until  the  pus  finds  external  vent.  An  hour  spent  in 
gaining  access  to  and  cleansing  such  canals  is  well  spent. 

The  patient  may  be  directed  to  make  suction  with  the  tongue 
to  create  a  vacuum  tending  to  draw  the  pus,  etc.,  into  the  canal. 
If  a  tight  joint  can  be  obtained  with  a  special  point  an  abscess  syringe 
may  have  its  plunger  drawn  back  to  create  the  vacuum.  This 
measure  is  not  necessary  when  prompt  relief  is  obtained  by  venting. 

The  canals  may  be  dried  and  an  anodyne  antiseptic,  such  as 
phenol  camphor  plus  menthol,  pumped  into  them.  If,  now,  pro- 
vision against  mastication  upon  the  elongated  tooth  be  made  by 
means  of  a  guard,  relief  is  tolerably  certain. 

Watkins^  has  used  "blue  light"  applied  from  a  16-candle  power 
blue-globed  electric  lamp  through  a  funnel  directly  upon  the  part. 
He  claims  relief  from  the  pain,  enabling  him  to  open  the  tooth 
previously  too  painful  to  be  operated  upon.  He  also  claims  that 
swelling  is  much  reduced  by  it,  in  some  cases  in  twenty  minutes. 
The  high  frequency  current  is  also  useful  in  this  connection. 

Patients  do  not  ordinarily  tolerate  the  rubber  dam  in  these  cases, 
and  as  the  tooth  should  be  left  open  it  need  not  be  used. 

A  guard  may  be  made  from  a  strip  of  rubber  dam  two  inches  long 
and  of  a  width  corresponding  to  the  distance  from  the  buccal  to  the 
lingual  gum  margins  and  folded  into  a  pad  of  the  width  of  the 
occlusal  face  of  the  tooth  to  be  covered.  Floss  silk  is  then  sewed 
through  this  in  such  a  manner  as  to  cause  it  to  tie  the  pad  over  the 
tooth,  the  silk  itself  encircling  the  neck  of  the  tooth.^  This  should 
be  attached  to  a  nearby  tooth,  and  will  insure  rest  of  the  affected 
pericementum  by  preventing  occlusion  upon  the  crown  (Fig.  549). 

1  Dental  Cosmos,  1905.  2  Flugg. 


600  SEPTIC  APICAL  PERICEMENTITIS 

Cold  antiphlogistics,  such  as  lead  water  and  laudanum  or  cata- 
plasma  kaolini,  should  be  applied  externally.  No  hot  external 
applications  should  be  used  in  abscess  cases,  as  they  may  cause  an 
external  fistula  to  be  formed. 

The  mouth  is  to  be  frequently  washed  with  an  antiseptic.  In 
simple  cases  with  prompt  relief  this  is  all  that  is  necessary;  in  marked 
cases  the  reduction  of  the  inflammatory  engorgement  should  be 
attempted  in  addition. 

Swedish  leeches  may  be  applied  to  the  gum,  or  a  cut  or  two  made 
in  the  gum  over  the  apex  of  the  tooth  will  allow  free  bloodletting 
and  drainage  of  the  excess  of  blood  in  the  pericementum.  A  hot  pedi- 
luvium  and  a  saline  cathartic  conjoined  are  useful  as  counterirritant 
derivatives,  and  the  latter  is  also  depletive,  reducing  the  volume  of 
the  blood.  The  hot  pediluvium  with  mustard  added  and  diaphoresis 
conjoined  are  also  useful.  Ten  grains  of  Dover's  powder  in  divided 
doses  in  hot  lemonade  are  given,  in  part,  while  the  pediluvium"  is 
being  administered,  and  the  patient  is  later  well  covered  up  in  bed. 

Fig.  649 


Rubber  dam  guard  for  use  in  pericementitis:  A,  roll  of  dam  threaded;  B,  guard  fitted 
over  tooth ;  tooth  eliminated  to  show  the  manner  in  which  the  silk  encircles  it. 

Quinin  in  doses  of  gr.  vj  is  given  as  a  febrifuge  and  to  limit  exu- 
dation, and  tincture  of  aconite,  two  drops  at  first,  and  one-half  drop 
each  half  hour  is  given  until  the  volume,  tension,  and  frequency  of 
the  pulse  are  reduced. 

If  syphilis  be  a  complication  in  these  cases,  potassium  iodid,  in 
doses  of  10  grains  each  three  hours,  is  useful  as  an  antagonist  of  its 
influence  and  as  a  nervous  sedative.  Unless  Dover's  powder  is  used, 
morphin  sulphate  in  blondes  and  morphin  bimeconate  in  brunettes 
(especially  those  with  blue  eyes),  or  any  persons  with  known  idio- 
syncrasies to  morphin,  should  be  administered  in  |  grain  doses, 
repeated  each  hour  up  to  f  grain.  When  great  suffering  renders  it 
necessary,  a  hypodermic  may  take  its  place.  When  used,  a  saline 
cathartic  should  be  given  the  following  morning.    Trigemin  is  useful. 

These  several  measures  are  to  be  regarded  as  the  abortive  treat- 
ment of  alveolar  abscess ;  they  apply  to  all  cases  if  seen  early  enough, 
and  will  in  the  majority  of  cases  prevent  the  disease  of  the  peri- 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     601 

cementum  passing  the  early  inflammatory  stages.  In  all  cases  the 
severity  of  the  inflammatory  process  is  lessened  in  proportion  to 
the  thoroughness  with  which  the  antiseptic  measures  are  applied, 
provided  that  in  the  attempt  at  such  application  no  septic  matter 
be  violently  thrust  through  the  apical  foramen,  especially  of  the  one 
of  a  multirooted  tooth  which  is  not  involved. 

The  Second  Stage  of  Acute  Apical  Abscess. — In  very  mild  stages  the 
pus  is  in  the  bone  and  the  infection  considered  more  virulent,  i.  e., 
the  germs  are  specially  active.  The  'abortive  treatment  should  first 
be  tried,  and  if  free  venting  of  pus  is  obtained  relief  is  usually  given. 
If  not  given  the  case  continues  to  the  third  stage.  If  bearable,  or 
the  surgical  method  be  impracticable,  a  dental  capsicum  plaster 
may  be  applied  to  the  gum  or  a  roasted  half-raisin  may  be  applied. 
Either  causes  an  inflammation  of  the  gum,  which  advances  the  tissue 
that  much  nearer  suppuration.  Thus  it  prepares  a  readily  invaded 
tissue  and  hastens  pointing.  The  contrary  eflFect  has  sometimes 
been  produced,  and  is  explained  upon  the  ground  that  the  increased 
amount  of  blood  has  increased  the  phagocytosis  and  destruction  of 
bacteria  or  has  stimulated  a  restoration  of  the  circulation,  possibly 
both.  Trigemin  is  a  useful  adjunct  when  the  pain  is  severe.  For 
the  purpose  of  hastening  suppuration,  calx  sulphurata,  |  grain  each 
hour,  is  useful.  It  also  sometimes  hastens  resolution.  It  is  proper 
to  denominate  this  the  expectant  treatment,  and  while,  perhaps, 
unsurgical,  at  times  permits  no  alternative  except  extraction. 

When  tolerable  or  imperative,  the  surgical  method  of  venting  the 
abscess  through  an  opening  in  the  gum  is  valuable.  The  apical 
region  is  located  as  nearly  as  possible  by  measuring  the  length  of  the 
tooth  with  a  probe  passed  into  the  canal  and  over  which  a  small 
piece  of  rubber  dam  is  slipped  as  a  guide.  This  is  laid  over  the 
crown  and  gum  and  a  tiny  drop  of  carbolic  acid  is  placed  just  above 
the  point  of  the  probe  as  a  guide.  A  vertical  cut  is  made  in  the 
gum  down  to  the  bone,  and  a  broad  spear  drill  is  driven  through  it 
into  the  abscess  tract.  Whether  this  shall  be  done  under  ethyl 
chlorid  refrigeration,  local  anesthesia,  or  short  general  anesthesia,  the 
operator  must  determine. 

A  gradual  perforation  is  useful  in  some  cases.  This  method, 
designed  by  Black,  consists  in  gradually  escharing  and  scratching 
the  gum  tissue.  Successive  applications  of  just  such  carbolic  acid 
as  adheres  to  the  point  only  of  a  sharply  serrated  plugger  are  made, 
followed  by  slight  scratching  only  so  that  blood  shall  not  be  drawn. 
In  this  way  the  bone  is  ultimately  reached. 

A  fresh  drop  of  acid  is  applied,  the  periosteum  scraped  away 
slightly,  and  the  drill  then  used. 


602 


SEPTIC  APICAL  PERICEMENTITIS 


A  Rollins  tubular  knife  (Fig.  550)  has  been  used  with  success  to 
remove  a  piece  of  gum,  after  which  the  drill  or  a  fine  trephine 
(Fig.  551)  is  used.  Some  acute  pain  may  follow  this  operation,  but 
usuall}''  lasts  only  a  short  time. 


Fig.  551 


Tubular  knives. 


Walker- Younger  trephines. 


If  antiseptics  are  used  to  syringe  out  the  abscess  cavity,  it  is  better 
to  use  a  mixture  of  six  parts  hamamelis  (aqueous)  and  one  part 
listerine  as  a  partial  sedative.  The  use  of  hydrogen  dioxid  is  often 
very  painful,  owing  to  the  rapid  reaction  with  the  blood  present,  and 
as  it  sometimes  also  drives  the  infective  material  into  remote  parts 
without  disinfecting  it,  its  use  in  this  connection  is  not  without 
danger,  and  should  be  avoided. 

It  has  been  a  subject  of  controversy  whether  a  tooth  should  be 
extracted  while  the  abscess  is  in  the  second  stage.  It  has  been 
claimed  that  the  continuation  of  pus  formation  after  extraction 
renders  the  state  of  the  patient  worse  than  before  extracted. 

This  occurrence  is  comparatively  infrequently  seen,  and  is,  of 
course,  due  either  to  the  retention  of  some  pyogenic  organisms 
beneath  the  clot  which  forms  in  the  alveolus  or  the  infection  of  the 
parts  by  extraneous  organisms. 

The  retention  of  the  tooth  until  a  fistula  forms  would  also  confine 
the  bacteria  for  the  time. 

Unquestionably  metastatic  infections  have  appeared  as  the  result 
of  persistent  local  infection  following  tooth  extraction,  the  avenue 
being  the  lymphatics;  therefore,  in  cases  of  extraction  during  the 
second  stage  of  pus  formation  the  alveolus  should  be  forcibly  syringed 
for  ten  minutes  with  the  above  listerine  solution.  If  it  be  thought 
desirable  to  repeat  the  syringing,  a  tent  of  antiseptic  gauze  may 
be  gently  carried  to  the  apex  of  the  alveolus  and  left.    This  tent 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     603 

may  be  removed  to  permit  syringing,  and  should  never  be  left  long 
at  any  one  time,  as  septic  inflammation  of  the  alveolar  walls  may  occur. 
It  also  does  not  drain  pus  readily,  so  it  might  cause  an  abscess  if 
left  too  long. 

In  cases  of  this  kind  oral  sterilization  and  anti-infective  systemic 
medication  are  of  importance.  As  soon  as  improvement  is  noted  the 
tent  should  be  removed,  the  alveolus  sterilized  as  before,  and  a  new 
•clot  induced  by  a  curetting  of  the  walls.  The  case  should  now  pro- 
ceed as  any  ordinary  extraction;  if  not,  it  should  be  treated  as  for 
dry  socket  (which  see). 

In  a  reply  to  a  circular  letter  of  questions  regarding  this  point, 
Black,  Kirk,  Ottolengui,  Hoffheinz,  and  Schamburg  all  favored 
extraction  as  a  means  of  removal  of  the  cause  and  as  a  less  evil  than 
allowing  the  tooth  to  remain  enclosing  the  bacteria,  which,  if  cap- 
able of  producing  septicemia,  it  would  do  if  allowed  to  remain.  They 
are  therefore  in  agreement  with  the  editor's  position  taken  in  the 
second  edition  of  this  work  (1904).  Brown  argues  the  difficulty  of 
decision  in  an  individual  case.  All  are  practically  opposed  to  the 
idea  that  pneumonia  is  more  likely  to  result  from  postextraction 
sepsis  than  septicemia,  Morris^  having  taken  the  position  that 
pneumonia  resulted  from  extractions  in  this  condition.  Each  and 
all  advised  careful  ante-  and  postextraction  antisepsis. 

The  editor  has  had  quite  a  number  of  cases  of  necrosis  (necrotic 
dry  socket)  following  extractions  at  the  hands  of  specialists,  and 
believes  they  and  he  should  have  been  more  watchful  in  these  cases, 
and  that  in  most  cases  a  strong  solution  of  potassium  permanganate 
should  be  used  as  a  wash  before  and  after  extraction,  or  tincture 
of  iodin  be  locally  applied,  especially  in  cases  requiring  laceration 
of  the  gum.  Antiseptic  spraying  of  the  alveolus,  etc.,  is  a  reliable 
measure.  In  one  case  of  extraction  of  a  lower  third  molar  opera- 
tion under  anesthesia  for  prevention  of  progressive  necrosis  became 
necessary.  The  making  of  a  cautious  diagnosis  and  awaiting  the 
proper  time,  as  recommended  by  Mitchell,  is  a  physical  impossi- 
bility unless  one  await  the  third  stage  or  a  fistula  or  general  infection, 
as  in  this  state  the  bacteria  are  considered  virulent,  especially  while 
bone  solution  is  in  progress. 

The  Third  Stage  of  Acute  Apical  Abscess. — In  this  stage  the  pus 
has  found  its  way  through  or  beneath  the  periosteum  on  the  outside 
of  the  bone;  therefore  its  germs  are  engaged  in  liquefying  the  gum 
tissue  or  in  unusual  location  the  mucosa  or  muscular  tissue  of  the 
part.     Except  in  these .  cases  the  gum  is  tumefied,  a  hard,  circum- 

»  Mitchell:  Dental  Cosmos,  1907,  p.  713. 


604  SEPTIC  APICAL  PERICEMENTITIS 

scribed,  inflamed  nodule  indicating  pus  near  the  bone,  a  soft,  more 
generally  diffused  swelling  indicating  more  superficially  located  pus, 
while  a  soft  yellow  or  yellowish-pink  tumefaction  indicates  pointing. 
In  all  these  cases  the  indication  is  for  a  surgical  opening  of  the  gum 
rather  than  the  opening  of  the  tooth.  The  part  should  be  gently 
disinfected  with  tincture  of  iodin  on  a  ball  of  cotton,  and  a  sharp 
bistoury  should  be  boldly  driven  to  the  bone,  with  the  cutting  edge 
turned  toward  the  occlusal.  The  lip  or  cheek  is  to  be  drawn  well 
away  to  avoid  injuring  the  coronoid,  buccal,  or  facial  artery.  A  cut 
about  a  half  to  three-quarters  of  an  inch  in  length  is  rapidly  made  by 
sweeping  the  edge  and  point  downward  occlusally.  Too  deep  lancing 
upon  the  hard  palate  may  injure  the  posterior  palatine  artery. 

As  this  is  usually  painful,  it  is  better  to  refrigerate  the  gum  with 
ethyl  chlorid  or  operate  under  short  general  anesthesia,  e.  g.,  nitrous 
oxid  or  the  first  impression  of  ether.  Novocain  is  only  useful  in  the 
case  of  deep-seated  pus  injected  into  the  more  healthy  tissue.  Next, 
the  abscess  tract  is  to  be  gently  washed  out  with  a  diluted  hama- 
melis  solution,  preferably  warmed.  Fairly  hot  water  containing  an 
antiseptic  also  gives  relief. 

If  the  abscess  has  been  deep-seated  it  is  well  to  introduce  a  fine 
tent  of  antiseptic  gauze  through  the  opening  into  the  abscess  tract 
to  prevent  the  too  rapid  healing  of  the  external  orifice  which  is  apt 
to  occur,  owing  to  the  approximation  of  the  lips  of  the  wound  pro- 
duced by  cheek  pressure.  This  healing  sometimes  permits  a  second 
collection  of  pus.  The  tent  should  be  removed  not  later  than  the 
next  day,  the  abscess  tract  disinfected  again,  possibly  with  a  mer- 
curic chlorid  solution,  and  the  tent  replaced.  At  this  time  the  tooth 
should  be  opened  and  disinfected  if  not  tolerable  at  the  first  sitting. 
When  this  is  tolerable  the  crown  may  be  tapped  and  formocresol 
sealed  in  the  pulp  chamber,  just  before  the  operation  of  lancing,  in 
order  to  permit  disinfection  and  thus  limit  pus  formation  and  to  save 
time.  Tents  in  aveoli  should  never  be  left  long  at  a  time,  as  they 
become  septic  and  may  cause  necrotic  conditions  of  the  alveolus. 

The  patient  should  always  be  cautioned  to  remove  the  tent  if 
swelling  return,  as  this  indicates  a  stoppage  of  the  vent,  with  collec- 
tion of  pus. 

When  diffuse  cellulitis  with  marked  febrile  disturbance  passing 
into  the  adynamic  type  is  produced,  one  should  fear  the  infection 
with  Streptococcus  pyogenes  and  treat  not  only  localh^,  but  use 
blood  germicides  against  a  possible  septicemia.  In  these  cases  there 
is  little  pus  formed  compared  with  the  area  involved. 

As  a  preventive  of  possible  blood  infection  the  following  may  be 
administered : 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     605 

IJ — Hydrargyri  bichloridi gr.j 

Tincturae  ferri  chloridi f3J — M. 

Sig. — ^Twenty  drops  in  water  four  times  a  day. 

The  editor  employed  this  remedy  with  markedly  beneficial  effect, 
while  suffering  from  a  very  severe  abscess  about  the  finger-nail,  due 
to  infection  by  the  Streptococcus  pyogenes  and  associated  with 
lymphangitis  extending  as  a  bright  red  streak  into  the  axilla. 

If  the  adynamia  and  other  symptoms  be  progressive,  medical 
cooperation  should  be  obtained  to  divide  the  responsibility  and  to 
afford  every  means  possible  toward  the  cure.  The  extraction  of  the 
tooth  followed  by  sterilization  and  curettement  of  the  part,  and  the 
use  of  streptococcus  antitoxin  or  vaccine  conjoined  with  the 
sustention  of  the  vital  powers  by  nutritious  predigested  food  and 
alcohol  is  logical.  In  even  ordinarily  severe  cases  not  of  this  variety 
and  there  will  be  some  fever  due  to  the  toxin  absorbed,  and  the  pain 
loss  of  sleep  and  appetite  will  cause  physical  debility.      (See  p.  149.) 

For  this  there  is  nothing  better  than  the  following,  as  tonic,  anti- 
septic, and  antipyretic: 

IJ— Saloli, 

Quininse  sulphatis  (vel  hydrochloratis)        .      .      .      .   aa     gr.  Ix 
M.  et  fiant  capsulas  no.  xx. 
Sig. — -Take  one  four  to  six  times  daily,  before  meals  when  near  them. 

Or, 

I^ — Quininse  sulphatis gr.  xxx 

Acetanilidi gr.  xxiv 

Caffeinse  citratis    .      .      .  , gr.  iij 

M.  et  fiant  pil.  no.  xij. 

Sig. — One  every  hour.     (Endelmann.) 

The  facial  swelling  resolves  with  the  cure  of  the  abscess  or  its  proper 
venting,  but  may  be  assisted  by  cold  applications  or  cataplasma 
kaolini  to  the  outside  of  the  face  and  by  gentle  massage  by  the 
patient  or  nurse. 

As  a  means  of  reducing  swelling,  vibratory  massage  is  useful.  A 
simple  appliance  for  this  purpose,  devised  by  W.  H.  Mitchell,^ 
consists  of  a  cam-like  piece  of  metal  perforated  at  its  smaller  end  for 
mounting  upon  a  screw  mandril;  it  is  held  in  the  dental  hand  piece 
strapped  to  the  hand  as  shown.  Its  centrifugal  force  imparts  a 
vibratory  motion  to  the  hand  which  can  be  utilized  for  massage  with 
the  finger  tips,  or  by  holding  in  the  hand  an  instrument  containing 
upon  its  end  a  soft  rubber  cup.  The  part  to  be  massaged  should 
be  lubricated  with  vaselin  (Figs.  552  and  553). 

1  Dental  Brief,  1908;  Academy  of  Stomatology. 


606 


SEPTIC  APICAL  PERICEMENTITIS 


The  heat  of  a  large  electric  lamp  concentrated  upon  the  face  from 
a  short  distance  and  followed  by  massage  is  also  useful  in  facial 
swellings  due  to  cellulitis. 


Fig.  552 


Fig.  553 


W. 


H.    Mitchell's   vibrator   strapped    to 
hand. 


W.  H.  Mitchell's  vibrator  a,nd  rubber 
cap   applicator. 


Under  no  circumstances  should  hot  poultices  be  applied  to  the 
outside  of  the  face,  as  a  discharge  of  pus  in  that  direction  will  cause 
a  disfiguring  scar.  If  an  abscess  threaten  to  open  externally,  the 
abscess  should  be  opened  by  an  incision  made  from  a  point  within 
the  mouth,  and,  after  sterilization  of  the  tract,  a  drainage  tent  of 
antiseptic  gauze  should  be  introduced  nearly  to  the  bottom  of  the 
pus  cavity.  This  should  be  removed  daily,  the  abscess  cavity  steril- 
ized, and  the  tent  renewed.  An  antiphlogistic  compress  should  be 
applied  to  the  face.  The  principal  object  sought  is  the  mechanical 
apposition  of  the  walls  of  the  abscess  cavity  at  the  dependent  or 
external  portion,  in  order  that  these  shall  unite  by  granulation  and 
that  the  fistula  shall  in  this  manner  become  an  ordinary  one.  The 
patient  should  lie  in  a  position  to  counteract  the  natural  effect  of 
gravitation. 

After  lancing,  the  mouth  should  be  kept  well  sterilized  by  frequent 
sprays  or  gargles  of  hydrogen  dioxid,  which  may  be  diluted  to  one- 
third  strength  with  water — i.  e.,  to  a  1  per  cent,  solution. 

If,  in  connection  with  the  lower  third  molar,  marked  swelling  be 
observed  in  the  submaxillary  triangle,  free  incision  of  the  tissues  of 


DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX     607 

the  floor  of  the  mouth  should  be  made  at  the  angle  of  junction  with 
the  bone.  The  cut  should  be  made  close  to  the  bone  and  toward  it, 
but  not  too  deep,  lest  the  mylohyoid  artery  or  nerve  be  injured. 

The  deep  lancing  of  an  abscess  upon  the  hard  palate  may  cause 
a  cut  to  be  made  in  the  posterior  palatine  artery.  External  to  the 
jaws  the  facial  and  coronoid  arteries  are  to  be  considered.  Keeping 
close  to  the  alveolar  process  while  the  cheek  is  pulled  out  renders 
the  operation  safe. 

It  is  ever  to  be  borne  in  mind  that  so  long  as  the  cause  of  infection 
remains  pus  formation  continues,  and  so  long  as  pus  forms  tissue 
destruction  is  in  progress;  furthermore,  in  proportion  to  the  amount 
of  tissue  loss  perfect  recovery  after  alveolar  abscess  is  delayed  or 
imperfect. 

While  it  is  the  clinical  experience  of  nearly  every  operator  that 
a  tooth  and  adjacent  structures  may  recover  from  inflammation 
which  involves  not  only  the  first  tooth  attacked,  but  by  an  extension 
of  the  inflammatory  process  involves  the  general  periosteum  and 
neighboring  teeth,  provided  the  case  receive  prompt  and  decisive 
surgical  treatment,  yet  the  danger  of  necrosis  and  septicemia  in 
prolonged  cases  is  always  imminent.  When  the  general  periosteum 
is  involved,  as  shown  by  extensive  boggy  swelling  in  the  mouth,  if 
several  free  incisions  carried  to  the  bone  do  not  afford  prompt  relief, 
the  tooth  which  is  the  centre  of  infection  should  be  promptly  ex- 
tracted. If,  in  the  continued  course  of  the  pericementitis,  chills, 
followed  by  fever,  a  coated  tongue,  and  much  physical  depression 
occur,  a  general  infection  is  to  be  feared,  and  no  time  should  be  lost 
in  sterilizing  the  mouth,  extracting  the  tooth,  and  subjecting  the 
socket  to  free  spraying  with  antiseptics.  Systemic  treatment  is  to 
be  given  (see  p.  605). 

In  cachectic  individuals  acute  abscesses  may  cause  inflammation 
of  the  deeper  tissues  and  of  the  periosteum  as  well,  and  extensive 
necrosis  may  occur.  The  after  treatment  of  acute  apical  abscess 
which  has  been  relieved  by  abortion  is  exactly  that  of  moist  gangrene 
or  of  chronic  abscess  without  fistula  (which  see).  In  very  mild 
cases  the  formaldehyd  treatment  may  be  instituted  at  once.  In 
severe  cases  it  is  better  to  allow  drainage  for  a  day  or  two.  When 
the  relief  has  been  afforded  by  lancing  the  treatment  is  as  for  chronic 
abscess  with  a  fistula  (see  p.  618). 

Acute  septic  apical  pericementitis  may  occur  on  a  temporary  tooth, 
most  frequently  a  temporary  molar.  The  symptoms  and  pathology 
are  the  same,  except  that  the  looser  character  of  the  alveolar  struc- 
ture seems  to  frequently  permit  the  abscess  to  assume  the  chronic 
form  before  the  dentist  is  consulted.     Children  often  hide  these 


608  SEPTIC  APICAL  PERICEMENTITIS 

conditions  from  their  elders  out  of  fear  of  the  dentist.  In  strumous 
children  the  inflammation  may  be  spreading  and  the  lymphatic 
glands  may  be  involved.  There  may  also  be  some  symptoms  of 
septic  intoxication  evidenced  by  chills  accompanied  by  fever,  etc. 
These  cases  require  an  opening  of  the  abscess,  sterilization  of  the 
part,  and  attention  to  the  systemic  condition.  If  seen  in  the  acute 
stage  the  treatment  is  the  same  as  for  the  permanent  teeth,  unless 
the  disease  occur  shortly  before  the  date  for  eruption  of  the  per- 
manent successor,  when  the  temporary  tooth  should  be  extracted, 
If  treated,  the  canals  should  be  filled  with  materials  which  can  be 
resorbed  by  the  tissues,  such  as  paraffin  or  wax  with  aristol,  para- 
form,  or  thymol  (Fig.  587). 

As  soon  as  the  pus  escapes,  the  condition  of  chronic  apical  abscess 
is  established. 


CHAPTER  XX. 

CHRONIC  SEPTIC,  PURULENT,  APICAL  PERICEMEN- 
TITIS (CHRONIC  APICAL  ABSCESS) 

By  this  title  is  meant  a  condition  of  apical  pericementitis  due  to 
septic  influences  in  which  pus  is  continuously  formed  at  the  expense 
of  the  apical  pericementum  and  contiguous  tissues.  It  is  the  usual 
outcome  of  acute  apical  abscess,  and  is  established  as  soon  as  the 
pus  finds  vent  either  through  the  gum  as  a  natural  or  operative 
result,  or  through  the  root  canal  as  the  result  of  opening  the  canal. 

These  two  avenues  of  pus  escape  give  the  two  clinical  conditions  of 
(1)  chronic  apical  abscess  discharging  via  the  root  canal;  (2)  chronic 
apical  abscess  with  fistula:  (3)  a  third  condition  of  latent' chronic 
apical  abscess  (true  blind  abscess)  with  absorption  of  pus  by  the 
tissue  may  exist. 


CHRONIC  APICAL  ABSCESS  DISCHARGING  VIA  THE 
ROOT  CANAL. 

Pathology  and  Morbid  Anatomy. — First  Grade. — Upon  abortion  of 
an  acute  abscess  in  the  first  stage  the  pressure  of  pus  upon  the  apical 
tissues  is  released,  and,  as  a  rule,  the  walls  of  the  abscess  cavity 
throw  out  granulations  which  fill  it.  This  tissue  tends  to  organize 
into  more  or  less  healthy  tissue  (cicatricial  tissue).  The  bacteria 
are  killed  out  except  at  that  part  represented  by  immediate  contact 
with  the  root  foramen;  at  this  point  the  tissues  are  infected  and 
some  molecular  loss  of  tissue  as  pus  may  occur.  A  limited  loss  of 
granulation  tissue  by  pus  formation  is  compensated  for  by  the 
formation  of  new  granulations.  The  conditions  are  almost  analogous 
to  those  existing  in  moist  gangrene  of  the  pulp,  and  require  analogous 
treatment. 

Second  Grade. — If  the  abortion  of  the  abscess  has  only  partly 
permitted  the  pus  to  drain,  or  the  alveolar  walls  or  crypts  of  the 
abscess  wall  remain  infected,  the  pus  will  continue  to  form  and 
escape  in  some  degree  ma  the  canal.  If  the  tooth  now  be  extracted, 
a  small  abscess  sac  will  be  found  upon  the  root  end.  If  opened, 
39  (609) 


610     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 


Fig.  554 


Chronic  apical  abscess 
third  grade:  B,  abscess 
sac  containing  a  central 
pus  cavity;  D,  apex  of 
root;  C,  canal  containing 
pus. 


this  will  be  seen  to  be  a  mass  of  fibrovascular  tissue  (inflamed  peri- 
cemental apical  tissue)  having  a  central  lumen  connecting  with  the 
root  canal  (the  abscess  cavity). 

Third  Grade. — With  partial  vent  to  the  pus  formed,  the  abscess 
cavity  of  the  second  grade  may  enlarge,  involve  the  bony  walls  of 
the  alveolus,  and  the  soft  tissues  then  pro- 
liferate to  such  an  extent  that  they  finally 
organize  into  a  large,  fibrous,  vascular  sac 
attached  to  the  tooth.  This  sac  has  the 
central  pus  cavity  before  described,  which  is 
connected  with  the  pulp  canal.  It  may  be 
a  half-inch  or  more  in  length  (Fig.  554), 
and  may  be  extracted  with  the  tooth  or 
may  be  left  attached  to  the  bone.  It  neces- 
sarily occupies  in  the  latter  a  cavity  of  a  size 
corresponding  to  its  own  bulk.  As  its  inner 
walls  are  infected,  extraction  without  its 
removal  leaves  an  infected  area,  which  must 
be  disinfected  or  a  secondary  acute  abscess 
may  result.  (See  p.  603.)  One  case  which 
had  given  only  slight  uneasiness  owing  to  partial  vent,  was  treated 
at  two  o'clock  and  the  tooth  extracted  at  midnight,  had  the  appear- 
ance shown  in  Fig.  554. 

Fourth  Grade. — Instead  of  organizing,  the  fibrovascular  tissue 
may  be  liquefied  into  pus.  The  root  apex  becomes  denuded  for  a 
distance  about  the  apical  foramen.  Pus  collects  about  the  apex  of 
the  root  and  rests  upon  the  bone,  owing  to  the  influence  of  gravity. 
The  bone  is  thus  infected,  inflamed,  and  further  liquefied,  while 
necessarily  the  abscess  cavity  enlarges.  If  a  bistoury  be  thrust 
through  the  labial  alveolar  wall  in  such  a  case,  as  shown  in  Fig.  555, 
but  slight  resistance  will  need  to  be  overcome.  In  the  lower  jaw  the 
tendency  is  to  burrow  into  the  cancellated  tissue  of  the  bone  away 
from  the  tooth,  so  that  destruction  of  the  pericementum  may  not 
be  very  extensive.  In  the  upper  jaw  the  tendency  is  to  spread 
along  the  pericementum  and  into  the  cancellated  bone,  so  that  the 
cavities  of  chronic  abscess  upon  the  upper  anterior  teeth  particularly 
may  cause  extensive  excavation  in  the  palatal  process  of  the  superior 
maxillary  bone  (Fig.  557).  The  pus  may  burrow  in  irregular  and 
circuitous  directions  until  it  finds  external  vent. 

In  long-established  cases  deposits  of  pus  calculi  (serumal)  may 
form  upon  the  root  end  (Fig.  558).  The  cement  corpuscles  of  the 
apical  cementum  may  die  and  the  root  tissue  itself  become  infected. 
In  other  cases  resorption  of  the  root  end  occurs.     (See  Resorption.) 


CHRONIC  APICAL  ABSCESS 


611 


Symptoms. — In  all  of  these  cases  the  formations  are  gradual,  owing 
to  the  partial  vent,  and  it  may  be  that  no  pain  beyond  a  slight 


Fig.  555 


Fig.  556 


Chronic  abscess  on  upper  incisor,  showing 
tendency  of  pus  progressively  to  destroy  peri- 
cementum, owing  to  the  influence  of  gravity. 


Chronic  abscess  upon  lower  tooth , 
showing  tendency  of  pus  to  sink 
into  the  substance  of  the  lower 
maxilla,  owing  to  the  influence  of 
gravity. 


gnawing  or  feeling  of  fulness  or  an  occasional  reflex  pain  may  occur. 
If  for  any  reason  the  vent  become  occluded,  the  pus  formation 
becomes  rapid  and  an  acute  abscess  is  set  up,  which  may  be  painful 


Fig  557. 


Fig.  558 


Chronic  apical  abscess  discharging 
through  the  hard  palate  and  threatening 
to  discharge  labially. 


Chronic  abscess,  showing  de- 
nudation of  apex  of  root  (a  to  fe), 
with  deposits  of  calculi  (a)  upon 
cementum. 


or  not,  according  to  the  amount  of  tension  produced  before  discharge 
of  the  pus.    Aside  from  this,  the  gum  color  at  the  apex  is  somewhat 


612     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

deepened,  the  tooth  is  slightly  loosened,  and  slightly  tender  to 
percussion.    Signs  of  previous  moist  gangrene  are  in  evidence. 

Diagnosis. — The  passage,  without  production  of  sensation,  of  an 
undue  length  of  fine  probe  into  a  canal  is  evidence  of  destruction  of 
apical  tissue  and  a  guide  to  its  probable  extent. 

An  extensively  inflamed  gum  tissue  over  the  apex  indicates  a 
probable  approach  of  pus  formation  to  gum  tissue.  The  presence 
of  pus  in  the  canal  or  upon  several  dry  cottons  introduced  for  absorb- 
ent purposes  is  diagnostic.  If  pus  be  not  seen,  and  the  canal  be 
thoroughly  sterilized  and  dressed  with  an  antiseptic,  the  supervention 
of  an  acute  abscess  affords  evidence  of  the  presence  of  an  abscess 
sac  or  cavity.    The  x-rays  afford  a  means  of  diagnosis  (Fig.  571). 

Prognosis. — The  prognosis  is  favorable  to  a  cure  in  nearly  all  of 
these  cases,  provided  thorough  canal  asepsis  and  filling  can  be 
attained  and  the  abscess  cavity  can  be  drained  and  disinfected.  In 
cases  resisting  this  treatment,  a  fistula  must  be  established. 

Treatment. — The  first  and  second  grades  of  chronic  apical  abscess 
discharging  via  the  canal  may  be  treated  upon  exactly  the  same 
principles  which  are  involved  in  the  treatment  of  moist  gangrene 
of  the  pulp.  The  infection  is  considered  as  simply  more  deep  seated, 
so  that  it  is  necessary  to  pass  disinfectants  into  the  abscess  cavity 
with  two  objects  in  view:  (1)  To  destroy  the  bacteria  present;  (2) 
to  stimulate  the  tissues  to  granulative  activity.  The  canal  should  be 
scraped  and  the  foramen  very  slightly  enlarged  if  necessary  with  a 
fine  Donaldson  cleanser,  the  canal  having  been  flooded  with  10  per 
cent,  formalin  or  formocresol  as  an  antiseptic. 

If  necessary  the  root  canal  may  be  otherwise  enlarged.    (See  p.  545.) 

A  dressing  of  10  per  cent,  formalin  or  phenol-camphor  to  which  a 
little  menthol  and  a  drop  of  formaldehyd,  40  per  cent.,  have  been 
added,  or  formocresol,  should  be  loosely  placed  in  the  canal  and  the 
tooth  sealed  for  twenty-four  hours,  or,  if  the  tooth  has  been  very 
troublesome  and  is  still  tender,  a  soft  temporary  stopping  may  be  used 
and  the  patient  provided  with  instruments  suited  to  the  removal  of 
the  covering  and  the  cotton.  It  is  better  that  the  tooth  should  be  under 
the  control  of  the  patient.  At  the  next  sitting  the  cement  stoppings 
are  more  tightly  made.  The  Zieler-Hoffendahl  method  may  be  used 
to  sterilize  the  root  and  abscess,  then  the  dressing  is  sealed  in  for  a 
few  days  and  renewed  as  necessary,  being  made  continuously  tighter. 
(See  p.  613.)  When  no  pus  can  be  found  on  the  dressing  or  follow- 
ing it,  or  on  an  exploratory  cotton  twist,  and  there  is  no  odor,  the 
root  may  be  filled;  in  case  of  any  doubt  in  fine  roots,  with  a  removable 
material  such  as  forma-percha  on  cotton  or  the  paraform  alum 
paste  (p.  552),  which  may  remain  if  no  ill-results  follow.     A  tem- 


CHRONIC  APICAL  ABSCESS  613 

porary  crown  filling  of  gutta-percha  should  be  used  for  a  week  or 
two.  Each  change  of  dressing  should  be  preceded  by  sterilization 
of  the  cavity  and  bulb  of  the  pulp  chamber  with  a  strong  formalin 
solution  to  prevent  reinfection  of  the  apical  tissue  during  the  change, 
and  it  is  well  to  use  counterirritation  directly  after  the  root  filling. 

It  is  always  well  when  using  an  occlusal  opening  to  close  it  with 
amalgam  or  cement  after  the  first  tentative  dressing,  while  compres- 
sible dressings  are  in  place,  as  even  one  heavy  bite  upon  the  covering 
may  force  the  medicament  into  the  apical  tissue  and  renew  the 
irritation.  Slightly  countersinking  the  orifice  of  the  tap  will  pre- 
vent an  inward  thrust  of  a  rigid  covering  overlying  cotton  (Fig. 
532). 

Some  operators  prefer  to  leave  a  small  vent  in  the  temporary 
covering,  used  to  act  as  a  drain.  This,  however,  is  apt  to  prevent 
the  concentration  of  the  action  of  the  medicament  upon  the  apical 
tissue.  If  formaldehyd  be  irritant,  perforating  the  temporary 
stopping  with  a  pin  will  sometimes  relieve  the  pressure. 

If  pus  formation  persist  in  any  case  with  a  large  foramen  the  cotton 
may  either  be  protruding  from  the  root  and  keep  up  irritation  or 
fall  short  of  the  root  end  and  permit  pus  to  enter  the  canal,  and 
especially  if  no  pain  has  been  produced,  good  results  sometimes 
follow  a  departure  to  the  immediate  method  of  root  filling.  The 
canal  and  pus  cavity  are  resterilized  for  a  half-hour  using  formocresol, 
deliquesced  zinc  chlorid,  or  carbolic  acid  on  cotton  against  the  apical 
tissue,  and  the  canal  apex  is  then  filled  with  gutta-percha  or  oxy- 
chlorid  of  zinc.  The  tissues  are  expected  to  care  for  themselves. 
A  persistent  discharge  of  serum  or  of  glairy  lymph  is  indicative  of 
inflamed  aseptic  but  weeping  tissue,  and  requires  the  same  treat- 
ment.    (See  p.  579.) 

In  a  relatively  few  cases  teeth  cannot  be  closed  at  all  without  a 
recurrence  of  trouble  within  a  short  period,  which  trouble  is  usually 
reheved  by  opening  the  tooth.  The  repetition  of  this  is  annoying, 
and  in  some  cases  is  due  to  the  strength  of  medicaments  such  as 
formaldehyd,  which  should  be  modified  or  abandoned  for  sedative 
antiseptics  such  as  phenol-camphor  or  eugenol  plus  menthol.  In 
some  of  the  cases  the  gases  may  accumulate  more  rapidly  than 
disinfection  occurs.  In  other  cases  the  irritability  of  the  tissues 
seems  to  produce  intolerance  of  any  remedial  measures.  What  is 
known  as  ''systematic  stopping  and  unstopping"  seems  sometimes  to 
overcome  the  irritability  and  accustom  the  tissues  to  being  covered. 
The  system  consists  of  stopping  with  eugenol  and  menthol  or  modified 
formocresol  for  about  eight  hours,  or  from  morning  to  afternoon, 
then  venting  and  redressing  until  the  following  morning,  then  for 


614     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

twenty-four  hours,  then  forty-eight,  then   seventy-two,   etc.,   until 
the  tooth  stays  stopped. 

There  have  been  a  few  patients  who  cannot  seem  to  have  teeth 
"treated,"  nearly  all  cases  being  practical  failures  even  when  aseptic. 
Some  few  may  be  kept  in  comfort  for  a  while  with  permanent  vents, 
but  this  is  objectionable.  The  making  of  an  artificial  fistula  should 
be  attempted. 

Cyst  formation  occurs  owing  to  the  projection  of  an  aseptic  root 
filling  or  to  some  not  well  understood  cause;  a  cystic  swelling  may 
occur  over  the  root  of  a  tooth  and  have  its  origin  in  the  pericementum 
The  swelling  is  apt  to  be  bluish  about  its  margin,  and  has  a  clear, 
stretched  look  in  the  centre.  It  is  probably  due  to  a  collection  of 
fluid  in  some  portion  of  the  pericementum,  or  may  have  as  its  excitant 
a  portion  of  calculus  deposited  aseptically  in  the  pericementum. 
Indeed,  apart  from  infection,  it  may  be  that  cases  of  pericemental 
abscess,  discharging  merely  glairy  fluid,  are  cystic  swellings.  It  may, 
however,  be  in  relation  with  septic  canal  contents.     (See  p.  631.) 

In  such  a  case,  if  swelling  increase  or  be  persistent,  an  artificial 
fistula  must  be  established  (see  p.  601)  and  the  case  treated  as  a 
chronic  apical  abscess  with  fistula. 

In  the  third  and  fourth  grades  the  prognosis  for  treatment  by  way 
of  the  canal  is  not,  as  a  rule,  good,  but  if  desired  may  be  attempted. 
If,  however,  an  artificial  fistula  be  established,  the  ease  of  treatment 
is  greatly  increased.  The  case  is  then  treated  as  a  chronic  apical 
abscess  with  fistula. 

In  no  case  should  hydrogen  dioxid  be  forced  in  quantity  into  the 
pus  occupying  such  an  abscess  cavity  until  the  fistula  has  been  made, 
and  it  is  better  even  then  that  the  bulk  of  it  be  washed  out  with  warm 
water  before  applying  the  drug.  A  neglect  of  this  precaution  may 
bring  about  great  pain,  owing  to  the  rapid  reaction  of  the  hydrogen 
dioxid  with  the  pus  and  blood  present.  In  some  cases  hydrogen 
dioxid  has  forced  pus  into  remote  locations  without  destroying  it. 

CHRONIC  APICAL  ABSCESS  WITH  FISTULA. 

Morbid  Anatomy  and  Pathology. — This  form  of  chronic  abscess 
occurs  as  the  result  of  the  discharge  of  an  acute  abscess  through  the 
gum  or  other  part  of  the  surface  of  the  body,  and  whether  the  fistula 
has  naturally  occurred  or  been  artificially  established.  (The  interior 
of  the  mouth  or  other  cavity  exposed  to  contact  with  the  air  is 
considered  external  to  the  body  proper.) 

If  the  acute  abscess  has  been  severe  or  long  continued,  the  tissue 
destruction  may  be  great,  but,  as  a  rule,  granulation  promptly  sets 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA 


615 


in  and  the  walls  of  the  abscess  cavity  organize  into  cicatricial  tissue. 
From  the  interior  of  this  a  canal  (fistula  or  sinus)  lined  with  cica- 
tricial tissue  leads  to  the  surface,  the  pus  being  almost  constantly 
formed  at  the  expense  of  the  granulation  tissue,  which  is  as  constantly 
renewed. 

The  fistulous  opening,  as  a  rule,  appears  as  a  small  teat  of  inflamed 
tissue  located,  in  the  majority  of  cases,  upon  the  buccal  surface  of 
the  gum,  about  a  quarter  of  an  inch  below  the  apex  of  the  root  and 
slightl}^  distal  to  it — a  position  probably  determined  by  the  density 
of  the  tissues  surrounding  the  acute  abscess.  At  times  the  only 
evidence  of  a  fistula  is  a  small  spot  of  inflammation  surrounding  a 
minute  opening,  from  which  pus  exudes.  The  fistula  is  sometimes 
located  upon  the  lingual  surface  of  the  gum.     It  may  perforate  the 


Fig.  559 


Fig.  560 


Chronic  apical  abscess  on  mesial  root. 
Ultimate  result  of  a  pulp  capping.  Editor's 
practice.     (Skiagraph  by  Hagopian.) 

bone  of  the  hard  palate  and  open 
through  the  mucous  membrane  of 
the  roof  of  the  mouth  (Fig.  557). 
Instead  of  finding  exit  by  a  direct 
path  through  the  buccal  or  lingual 
alveolar  plate  and  gum,  the  pus 
may  burrow  along  the  length  of 
the  pericementum  and  discharge 
at  the  neck  of  the  tooth,  and  sim- 
ulate a  pyorrhea  pocket  (Figs.  542 
and  543) .  One-half  or  more  of  the 
lateral  aspect  of  the  pericementum 
may  remain  vital,  although  involved 
in  a  chronic  inflammation,  the  remainder  being  destroyed.  Not  in- 
frequently the  pus  burrows  along  the  surface  of  the  bone  and  dis- 
charges at  a  point  over  an  edentulous  portion  of  the  jaw.     This  is 


Chronic  alveolar  abscess  of  the  root 
of  a  lower  incisor,  with  abscess  cavity 
passing  through  the  body  of  the  bone 
and  discharging  on  the  skin  beneath 
the  chin:  a,  very  large  abscess  cavity; 
b,  mouth  of  the  fistula.     (Black.) 


616     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

common  to  a  lower  bicuspid.  It  may  burrow  in  the  direction  of 
the  apices  of  other  teeth,  destroy  their  pulps  and  thus  cause  an 
abscess,  having  added  causes  for  persistence. 

When  the  apices  of  the  roots  of  upper  posterior  teeth  lie  in  very 
close  proximity  to  the  floor  of  the  antrum,  perforation  of  this  floor 
may  occur  before  tissue  destruction  has  proceeded  far  enough  in 
other  directions  to  afford  escape  to  the  pus  (Fig.  545).  Extensive 
pus  accumulations  may  occur  in  the  antrum  in  consequence,  and 
when  the  tissues  in  the  antral  floor  are  affected,  other  teeth  may  be 
involved.  It  may  discharge  into  the  cavity,  in  connection  with 
acute  abscesses;  at  such  points  the  discharge  may  remain  persistent. 
Sometimes  the  discharge  occurs  through  the  canal  of  the  affected 
tooth;  the  canal  then  acts  as  a  fistula  (Fig.  538).     Upon  a  lower 


Fig.  561 


Fig.  562 


Fistula  passing  down  through  the  body  of 
the  lower  maxilla.     (Black.) 

tooth,  particularly  the  incisors,  the 
pus  may  burrow  downward  through  7 
the  cancellated  tissue  of  the  bone 
and  emerge  at  the  base  of  the  bone 
and  open  upon  the  face  (Figs.  560  and 
561). 

Chronic  alveolar  abscess   at  the 

In  other    cases    the    pus    may    per-  root    of    a    lower    incisor,    with    a 

forate    the     bone     and     find     passage  fistula  discharging  on  the  face  under 

.  the  chin:  a,  abscess  cavity  in  the 

along    the    SubmuSCUlar    tissue,     open-  bone;    b,  b,  b,   fistula  following   in 

ing     upon     the     face     or     neck     (Fig.  the  periosteuni  down  to  the  lower 

rnn\        mi  •  Pi  j»  margin  of  the  body  of  the  bone  and 

562).       Ihe     apices     of     the     roots     of  discharging  on  the  skin.   (Black.) 

teeth  lying    beneath    the    line  of  in- 
sertion of  the  mylohyoid  muscle  may  cause  an  abscess  to  open  in 
the  neck  cavity.     Cryer  records  a  case  where  an  abscess  opening 
upon  the  face  immediately  anterior  to  the  line  of  the  facial  artery 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  617 

was  traced  to  the  root  of  a  lower  molar;  the  direction  of  the  sinus 
is  shown  in  Fig.  563.  In  a  case  having  a  similar  anatomical  associa- 
tion the  pus  penetrated  the  bone  lingually,  was  encapsuled  beneath 
the  internal  pterygoid  muscle,  and  appeared  as  a  swelling  at  the 
inner  aspect  of  the  angle  of  the  jaw.  Another  case  dissected  along 
the  muscles  of  the  neck  and  discharged  at  the  clavicle.  Occasionally 
the  apices  of  the  roots  of  lower  molars  are  separated  from  the  inferior 
dental  canal  by  only  a  thin  lamina  of  bone,  so  that  discharge  into 
this  canal  may  occur  with  infiltration  along  the  vessels  and  nerves 
in  the  canal  (Fig.  254).  While  discharge  into  the  nasal  chamber 
is  most  frequently  associated  with  abscess  upon  the  central  incisors, 
abscesses  upon  molars  may  discharge  into  the  same  cavity. 

Cementum  infection  occurs  as  a  sequence  to  death  of  the  cement 
corpuscles  from  lack  of  nutrition.  Pus  calculi  may  also  form  on  the 
roots  in  the  long  continued  cases.  The  granulation  tissue  springing 
up  about  the  parts  has  a  resorbent  action  and  the  root  ends  are 
often  resorbed,  though  this  action  is  probably  to  an  extent  counter- 
acted by  the  alkalinity  of  the  pus.  The  formation  of  the  latter  may 
however,  be  in  abeyance  at  times. 

The  extent  of  tissue  destruction  varies  considerably,  but  is  usually 
greatest  in  dependent  parts,  gravity  influencing  the  burrowing  of 
the  pus. 

Symptoms  and  Diagnosis. — A  fistula  is  seen  upon  the  gum,  visible 
as  either  a  small  teat  of  flesh  (perhaps  pedunculated),  discharging 
pus,  or  as  a  tiny  orifice  in  the  gum  surrounded  by  inflamed  tissue, 
and  from  which  pus  may  be  squeezed  (Fig.  544).  As  a  rule,  a  soft 
silver  probe  may  be  passed  to  the  apex  of  a  nearby  root,  whether 
possessing  a  crown  or  embedded  in  the  bone.  In  case  of  an  external 
opening  upon  the  face  a  similar  procedure  shows  the  trouble  to  lie 
with  some  tooth  root.  The  a:-rays  will  sometimes  be  valuable  in 
determining  the  exact  location  of  the  abscess  cavity. 

Upon  the  teeth  themselves  but  four  conditions  may  cause  a  fistu- 
lous opening:  (1)  Moist  gangrene  of  the  pulp  or  its  equivalent  apical 
infection;  sometimes  the  sinus  is  at  the  oral  end  of  a  broken  root; 
(2)  septic  perforations,  apical  or  lateral;  (3)  a  pericemental  abscess 
(see  Pericemental  Abscess);  or  a  secondary  abscess  associated  with 
a  pyorrhea  pocket  (see  Pyorrhea  Alveolaris);  (4)  lateral  abscess 
about  a  third  molar  or  impacted  tooth. 

Aside  from  these,  the  probe  may  lead  to  carious  or  necrosed  bone, 
a  cyst,  or  a  subperiosteal  abscess  (maxillary  periostitis) . 

In  these  cases  the  probe  does  not  lead  to  a  root.  Carious  bone 
will  impart  a  honey-combed  sensation  to  an  excavator;  necrosed 
bone  will  be  exposed  and  firm,  or  the  sequestrum  will  be  in  evidence 


618     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

as  a  movable  body.  There  may  also  be  several  fistulas  and  extensive 
inflammation  of  the  tissue.  A  cyst  will  be  a  tumor  with  certain 
characteristics,  and  an  impacted  tooth  will  usually  impart  the  feel 
of  smooth  enamel  to  the  instrument,  though  the  enamel  may  at 
times  be  rough  at  certain  points.     An  embedded  root  will  be  movable, 


Fig.  564 


Abscess  with  tortuous  sinus,  open- 
ing upon  the  face:  A,  tissue  of  cheek; 
B,  floor  of  mouth;  C,  abscess  tract. 

Fig.  565 


Large  abscess  cavity  in  relation  with  a 
lateral  incisor,  complicated  by  an  im- 
pacted supernumerary  tooth  beneath  the 
nasal  spine.  (Philadelphia  Dental  College 
Museum.) 


and  will  present  the  dentin  and  its 
central  opening,  the  pulp  canal, 
as  diagnostic  features.  Maxillary 
periostitis  will,  as  a  rule,  have  a 
history  of  traumatism,  or  the  pre- 
vious use  of  a  probably  infected 
hypodermic  needle^  associated  with 
it.  In  all  cases  not  clearly  due  to  other  than  dental  causes,  evi- 
dence of  the  four  dental  conditions  mentioned  should  be  sought. 

Treatment. — In  cases  arising  from  sources  not  dental,  surgical 
interference  for  the  removal  of  the  cause  is  necessary.  This  may 
require  a  minor  or  major  operation,  according  to  the  case. 

In  the  purely  dental  cases  the  cause  must  also  be  removed.  If 
due  to  pericemental  abscess,  this  is  to  be  treated.     If  due  to  a  septic 


Abscess    and    resorption    at    apex. 
(Skiagraph  by  Lodge) 


Boenning,  Dental  Cosmos,  1902 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  619 

perforation  not  yielding  to  treatment  by  way  of  the  root  canal, 
the  fistula  may  be  enlarged,  packed  open  with  antiseptic  cotton  or 
gauze  applied  on  successive  days,  and  when  the  perforation  is  exposed 
it  may  be  filled  with  amalgam.  If  properly  done  the  fistula  should 
heal.  If  this  operation  be  impossible,  the  root  should  be  amputated 
at  a  point  between  the  perforation  and  the  crown.  If  the  perforation 
be  in  the  middle  or  cervical  third  of  the  root,  it  may  at  times  be 
treated  from  the  root  canal.  A  good  method  is  to  force  root-filling 
material  through  the  perforation  and  fistula  and  to  smooth  it  off 
through  the  sinus.  Stiff  oxychlorid  of  zinc  or  oxy phosphate  of 
copper  are  excellent.  If  incurable,  the  entire  root  must  be  amputated 
in  case  of  a  multirooted  tooth.  In  case  of  a  single-rooted  tooth 
the  tooth  must  be  extracted,  and  if  the  conditions  warrant  the, 
operation  the  root  may  be  perfectly  sterilized,  properly  filled,  and 
then  replanted  after  the  associated  abscess  cavity  has  been  surgically 
obliterated.     (See  p.  624.) 

In  the  cases  due  to  moist  gangrene  of  the  pulp  the  canals  must  be 
freely  entered,  the  apical  foramen  opened  with  Donaldson  or  other 
cleansers,  and  the  canals  and  abscess  tract  thoroughly  sterilized. 

The  canals  are  flooded  with  a  formaldehyd  solution,  mechanically 
enlarged,  and  if  possible  made  continuous  with  the  abscess  cavity. 
It  is  then  filled  with  hydrogen  dioxid.  With  a  Swiss  broach  upon 
which  cotton  is  wound  a  plunging  force  is  exerted  upon  the  fluid  in 
the  canal.  This  tends  to  drive  it  into  the  abscess  cavity  and  out  of 
the  fistula,  flushing  and  sterilizing  the  abscess  tract.  This  is  then 
repeated.  Antiseptic  liquid  soap  may  be  used.  If  this  simple  pro- 
cedure be  not  effective,  a  thread  of  cotton  saturated  with  carbolic 
acid  should  be  placed  in  the  canal.  Pressure  is  then  exerted  with 
gutta-percha,  as  in  pressure  anesthesia.  A  bit  of  cotton  roll  should 
be  used  to  guard  against  burning  the  tissues.  Phenolsulphonic  acid 
may  be  forced  through  the  apical  foramen  and  fistula  in  some  cases.^ 
This  dressing  may  be  left  until  the  next  visit.  A  third  method  con- 
sists of  filling  the  crown  cavity  with  gutta-percha  or  vulcanite 
rubber,  forcing  the  nozzle  of  an  abscess  syringe  through  the  mass, 
and  driving  down  the  piston  of  the  syringe.  In  all  these  procedures 
except  the  initial  sterilization,  the  unaffected  roots  of  multirooted 
teeth  are  to  be  avoided  so  far  as  possible,  as  undue  pressure  may 
excite  an  abscess     The  fistula  will  admit  the  nozzle  of  the  syringe, 

I  Acid  phenolsulphonic  consists  of  97  parts,  by  weight,  of  concentrated  sulphuric 
acid  and  93  parts,  by  weight,  of  phenol,  kept  at  100°  C.  for  about  twenty-four  hours 
to  produce  a  reaction,  when  suiBcient  distilled  water  is  added  to  make  the  liquid 
assay  about  80  per  cent,  of  phenolsulphonic  acid.  (Buckley,  Lilly.)  Prinz,  in  Cosmos, 
April,  1912,  gives  some  good  reasons  for  its  inferiority  for  any  purpose  to  sulphuric 
acid. 


620     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 


Fig.  566 


Fig.  567 


Minim  syringe. 


J.  N.  Farrar's  alveolar  abscess  syringe. 


Fig.  568 


Bulb  syringe. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  621 

which  may  be  used  to  jflush  out  the  abscess  tract  with  hydrogen 
dioxid. 

The  nozzle  of  a  hypodermic  needle  may  be  fitted  to  the  canal  by 
packing  wax,  temporary  stopping,  or  raw  vulcanite  about  it;  a  piece 
of  flexible  tubing  may  be  previously  stretched  over  the  free  end  and 
later  the  other  end  of  the  tubing  stripped  over  the  compressed-air 
syringe.  Medicaments  or  air  may  thus  be  blown  through  the  fistula. 
The  method  should  be  cautiously  used  in  fistulous  cases  only,  except 
for  reasons  well  known  by  the  operators  employing  them,  as  very 
painful  distention  of  the  cheek  may  occur.     (See  p.  576.) 

The  rubber  cup  shown  in  Fig.  569  may  be  used  as  a  vacuum  pump 
to  draw  the  pus  from  the  fistula  or  to  draw  medicaments  through 
the  canals. 

All  preliminary  work  having  been  done  as  well  as  possible,  formo- 
cresol  is  to  be  pumped  into  the  abscess  tract  and  the  canal  tempor- 
arily stopped  with  the  sam€  antiseptic  on  cotton.  With  this  treat- 
ment the  discharge  of  pus  should  cease  and  be  replaced  by  serum. 
It  is  good  practice  to  resterilize  the  canal  and  fill  it  as  soon  as  this 
result  is  noted,  or,  in  emergency  cases,  the  canal  may  be  filled  at 
the  first  sitting  after  prolonged  germicidal  work.  The  fistula  then 
will  probably  heal  uninterruptedly  in  the  vast  majority  of  cases. 
In  a  week  or  two  the  fistula  should  have  healed  if  attached  to  treat- 
able canals;  for  the  difficult  canals  subjected  to  germicides  only  more 
time  may  be  required,  but  healing  usually  eventually  occurs  owing 
to  the  removal  of  the  cause. 

If  the  abscess  cavity  does  not  heal  one  of  several  causes  may 
be  assigned:  (1)  The  crypts  in  the  walls  of  the  abscess  cavity  may 
require  further  disinfection;  (2)  the  cotton  in  the  canal  may  have 
absorbed  pus  formed  after  an  interval  of  antiseptic  influence  and 
may  keep  up  the  infection;  (3)  the  root  canal  may  not  be  explorable; 
(4)  the  root  end  may  be  encrusted  with  calculus,  or  the  cementum  be 
infected,  or  dead  bone  may  be  present. 

For  the  first  condition  the  canal  and  abscess  tract  may  be  treated 
with  10  per  cent,  zinc  chlorid,  or  mercuric  chlorid  may  be  added 
to  hydrogen  dioxid  (1  to  500  or  1  to  1000)  and  the  abscess  cavity 
syringed  out  at  intervals.  For  the  second  condition  a  non-absorbent 
dressing  should  be  used,  such  as  forma-percha,  or  the  root  apex 
may  be  permanently  filled  with  gutta-percha.  In  the  fine,  unex- 
plorable  canals  25  per  cent,  pyrozone  may  be  used  for  twenty-four 
hours,  as  though  bleaching  the  root,  or  Rhein's  cataphoric  method 
(see  p.  556)  may  be  employed.  In  some  cases  abscesses  require 
some  weeks  to  heal,  but  eventually  do  so,  particularly  if  the  abscess 
be  syringed  out  with  an  antiseptic  every  third  day  via  the  fistula, 


622     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

and  the  abscess  tract  filled  with  balsam  of  Peru  or  paraffin  and 
aristol.  Beck's  bismuth  paste  may  be  injected  for  skiagraphy  or  to 
stimulate  the  fistula.  Opening  the  fistula  daily  with  a  probe  or 
needle  aids  healing  from  the  bottom  out. 

Tissues  about  abscesses  have  an  inherent  tendency  to  repair;  cases 
of  long  standing  frequently  healing  promptly,  sometimes,  though  not 
often,  in  twenty-four  hours. ^ 

In  indolent  chronic  inflammation  the  use  of  a  small  gum  dry  cup 
with  vacuum  bulb  attached  may  be  used  for  five  or  ten  minutes 
at  a  time  several  times  a  day,  to  draw  fresh  blood  and  effusions 
into  the  inflamed  part.  The  opsonic  index  of  the  lymph  drawn 
in  is  said  to  be  raised  to  several  times  beyond  that  of  the  body  lymph, 
thus  rapidly  increasing  phagocytosis  in  the  part.  The  rubber  cup 
shown  in  Fig.  569  may  be  left  imperforate  and  furnished  the  patient 
for  this  purpose. 


Fig.  569 


Fig.  570 


Rubber  cup  to  be  used  as  a  Amputation  of  root  apex:  OG,  opening  in 

vacuum  cup.  the    gum    made    by    packing    fistula;  AC, 

abscess  cavity;  RF,  root  filling. 

For  the  fourth  class  of  cases  the  apical  foramen  should  be  sealed 
and  the  abscess  tract  syringed  once  a  week  with  25  per  cent,  sul- 
phuric acid,  the  mouth  and  clothing  being  properly  protected  by 
using  a  pad  of  cottonoid  over  the  fistula  and  needle  to  absorb  the 
excess.  This  dissolves  calculi  and  disinfects  dead  cementum.  It 
also  stimulates  the  soft  parts  to  a  granulative  action.  If  necessary 
the  patient  should  receive  appropriate  systemic  treatment,  especially 
if  anemic.  (See  p.  637.)  In  this  way  some  old  and  somewhat  obsti- 
nate cases  may  be  induced  to  heal.  In  some  cases  gravity  so  retains 
pus   in   abscess   cavities  that  granulation  is  interfered  with.     The 


1  Darby,  Proceedings  of  Academy  of  Stomatology,  Philadelphia,  1899. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA 


623 


instruction  of  the  patient  in  the  syringing  out  of  the  tract  with  a  mild 
antiseptic  several  times  a  day  is  of  great  value  in  that  it  removes 
pus  which  if  retained  w^ould  destroy  granulations.  Hydrogen  dioxid 
should  not  be  used  except  in  small  abscesses  as  it  may  cause  the 
forcing  of  pus  to  distant  areas.  ]\Iany  apparently  desperate  cases 
heal  of  their  own  accord  after  some  months.  Some  success  attends 
the  packing  of  a  root  with  a  thick  paste  of  iodoform  in  any  oil  after 
opening  the  root  as  far  as  possible.  Cases  in  which  a  canal  was  not 
explorable  for  any  considerable  distance  have  healed  after  this  treat- 
ment. The  .r-ray  application,  made  for  ten  or  twenty  seconds,  or  ski- 
agraphy seems  to  aid  the  healing  of  the  fistula.  The  high  frequency 
current  also  is  a  stimulant.  If  the  abscess  be  incurable  by  the 
above  method,  or  radical  measures  being  considered  better,  the  root 


Fig.  571 


Fig.  572 


Fig.  573 


A  skiagraph  of  apical 
abscess  cavity  about  two 
root  apices;  incurable 
by  ordinary  means. 


The  same  after  root 
amputation. 


The  same  thirty 
days  later,  showing 
a  certain  amount  of 
new  bone  formation. 
(Price.) 


end  may  be  amputated,  after  canal  filling  as  far  as  possible  with 
gutta-percha.  The  fistula  is  enlarged  and  packed  open  with  anti- 
septic gauze  or  cotton,  or  sandarac  varnish  dipped  into  powdered 
orthoform  applied  until  the  root  end  is  fairly  in  view.  After  steril- 
ization of  the  abscess  cavity  and  local  anesthesia,  a  dentate  fissure 
bur  or  a  Schamburg  surgical  bur  is  laid  upon  one  side  of  the  root  at 
the  level  of  the  healthy  tissue,  and  carried  laterally  with  a  sawing 
motion  until  the  root  end  is  separated.  It  may  readily  be  picked 
out.  If  the  root  can  be  correctly  located  without  packing  the  fistula 
the  part  may  be  anesthetized  and  a  portion  of  gum  may  be  cut  away 
with  a  tubular  knife,  or  an  incision  may  be  made,  after  which  a 
fissure  or  surgical  bur  may  be  used  to  cut  away  the  root.  Any 
necrosed  bone  may  be  removed  at  the  same  time.  A  skiagraph 
to  act  as  a  guide  is  necessary  when  the  fistula  is  not  packed  open. 


624     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

Necrosed  root  ends  may  occasionally  be  seen  projecting  through 
the  gum  and  alveolar  process  which  have  been  lost  above  them. 
They  should  be  removed  as  above  indicated.  Sometimes  salivary 
calculus  deposits  on  them. 

Antiseptic  gauze  or  cotton  saturated  with  balsam  of  Peru  should 
be  packed  into  the  abscess  cavity  after  operation  to  stimulate  granu- 
lation. The  quantity  of  gauze  should  be  gradually  lessened  until 
the  cavity  is  nearly  healed.  It  should  thereafter  be  kept  sterilized 
by  means  of  hydrogen  dioxid  until  the  cavity  has  healed.  An 
alternative  is  to  inject  into  the  cavity  Beck's  bismuth  paste: 

I^ — Bismuth  subnitrate 30  parts 

Vaselin 65  parts 

Paraffin 5  parts 

Wax 5  parts 

Mix  while  boiling.  ' 

which  excludes  septic  moisture,  is  antiseptic,  and  stimulates  granu- 
lation. Stimulation  by  means  of  fused  silver  nitrate  or  sulphuric 
acid  or  scarification  is  at  times  necessary.  Bone  should  gradually 
be  deposited  about  the  roots  (Figs.  571,  572,  and  573).  Failure 
indicates  some  condition  of  sepsis;  presumably  the  amputation  has 
not  included  all  septic  root  or  the  canal  filling  is  defective. 

A  still  more  radical  method  of  surgical  treatment  involves  the 
extraction  and  replantation  of  the  root,  if  worth  while.  The  mouth 
is  sterilized  and  the  tooth  extracted,  care  beng  taken  not  to  injure 
the  enamel  with  the  forceps.  It  is  then  placed  in  a  1  to  1000  solu- 
tion of  mercuric  chlorid  at  120°  F.,  or  phenol  sodique,  20  per  cent. 
The  apex  of  the  alveolus  is  in  the  meantime  sterilized  with  hydrogen 
dioxid  plus  mercuric  chlorid  and  thoroughly  curetted.  Bleeding  is 
checked  with  the  same  solution  or  phenol  sodique,  20  per  cent., 
and  a  tampon  of  cotton  saturated  with  the  latter  is  packed  into 
the  alveolus.  The  replantation  may  be  deferred  for  a  few  days  if 
the  parts  are  badly  infected.     In  such  case  granulation  is  permitted. 

Returning  to  the  tooth,  the  apex  is  cut  off  slightly  beyond  the 
denuded  area  and  smoothed;  the  pulp  canal  is  well  opened  from  the 
apex,  all  debris  removed  from  it,  and  it  is  then  well  sterilized  with 
sodium  dioxid  or  25  per  cent,  pyrozone.  The  canal  is  then  dried 
and  filled  entirely  with  gutta-percha,  or  partly  with  gutta-percha 
and  the  operation  completed  with  gold,  which  is  nicely  smoothed. 
The  tooth  should  be  handled  in  an  aseptic  napkin  or  one  wet  with 
the  antiseptic,  and  when  ready  should  be  returned  to  the  sterilizing 
solution.  All  being  ready,  the  tampon  or  granulations  are  removed, 
the  tooth  washed  in  sterile  water  and  replaced  in  its  socket,  and  a 
previously  prepared  retaining  appliance  cemented  to  place.     This 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  625 

should  remain  for  six  weeks  and  be  replaced  should  indications 
demand  it.  If  the  tooth  be  valueless  for  replantation  purposes, 
the  operation  of  transplantation  may  be  done  either  immediately 
after  extraction  of  the  offending  tooth  or  a  few  days  later.  The 
possibility  of.  resorption  of  the  root  after  plantations  should  have 
careful  consideration,  though  it  is  not  prohibitory. 

The  operation  of  transplantation  may  be  done  with  a  tooth  recently 
extracted  from  another  mouth  or  with  a  dried  tooth,  or,  preferably, 
one  kept  in  alcohol  and  glycerin,  which  many  extracting  specialists 
habitually  retain  to  oblige  applicants.  If  a  suitable  tooth  be  not 
obtainable,  a  root  may  have  a  crown  mounted  upon  it  in  such  manner 
as  to  have  an  open  joint  at  a  point  to  be  placed  beneath  the  gum 
line,  and  this  joint  should  be  filled  with  cohesive  gold  and  polished. 
The  tooth  root  is,  of  course,  sterilized  previous  to  and  after  the 
crown  mounting,  and  its  canal  should  have  been  thoroughly  filled 
with  gutta-percha.  Any  of  these  may  become  firm  if  thoroughly 
splinted  for  a  proper  length  of  time.  The  alveolus  should  be  made 
to  fit  the  root  snugly  by  means  of  a  bone  reamer.  The  operation 
of  implantation  differs  from  this  only  in  the  fact  that  it  is  done  where 
a  tooth  alveolus  has  been  obliterated  by  combined  absorption  and 
bone  formation,  as  after  extraction  (see  p.  142).  If  the  tooth  be 
not  lost  by  resorption,  it  is  probable  that  some  resorption  occurs — 
toleration  then  ensues  and  bony  deposition  in  the  bays  of  resorp- 
tion and  about  the  root  occurs.  Possibly  a  true  ankylosis  (which 
see)  may  occur. 

To  select  a  proper  tooth  make  a  model  and  bite  from  an  impression 
taken  before  extraction  or  immediately  thereafter,  cut  off  the  offend- 
ing tooth  from  the  model,  ream  out  a  socket  in  the  plaster ;  select 
tooth,  and  fit  in  place;  attach  with  a  little  soft  plaster,  the  model 
being  thoroughly  wet.  Construct  the  retaining  appliance,  remove 
the  tooth,  sterilize,  and  fill  the  root;  then  put  the  tooth  in  the 
sterilizing  agent  until  needed.  Mendel-Joseph  and  Dassonville'^ 
have  shown  that  in  case  of  removal  of  a  portion  of  the  pericementum 
the  lost  portion  may  be  regenerated. 

Greenfield'^  has  introduced  an  artificial  root  made  cribriform  of 
platinum  soldered  with  pure  gold.  Special  instruments  of  varied 
sizes  are  necessary  to  correspond  with  the  sizes  of  the  roots.  Under 
due  aseptic  precaution  the  gum  is  cut  with  a  tubular  knife,  and  the 
socket  drilled  with  a  circular  trephine,  which  preserves  a  core  of 
bone,  and  the  root  covered  with  Beck's  bismuth  paste  is  inserted. 
Later  a  crown  is  mounted  or  a  bridge  attachment  constructed. 

1  Dental  Cosmos,  1906,  p.  1059.  2  Ibid.,  April,  1913. 

40 


626     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

The  reader  is  referred  to  the  article  for  details.     The  editor  has  had 
no  experience  with  this  method. 


Fig.  574 


Fig.  575 


yft/O't^ 


m*» 


•99 


Tubular  knife  for 
cutting  gum. 

Fig.  576 


Trephine  with  central 
starter  later  removed. 


Fig.  577 


Fig.  578 


Trephine  with  cen- 
tral starter  removed. 

Fig.  579 


c 

Artificial    socket         Artificial  root  and 
drilled   in   bone,  a     crown  separated, 
core  being  left. 


Artificial  root 
with  crown  in 
place. 


Artificial    root    in 
place. 


Several  cases  of  fistulous  openings  into  the  antrum  have  been 
noted  by  canal  exploration  in  which  no  history  of  discomfort  from 
antral  empyema  could  be  obtained.  It  was  assumed  that  the  root 
ends  approximated  the  floor  of  the  antrum,  and  that  the  abscesses 
were  of  simple  chronic  type.  Such  cases  were  treated  upon  the 
common  principle  of  canal  antisepsis,  flushing  the  abscess  tract 
with  an  antiseptic,  and  filling  the  canals.  The  antral  condition 
was  explained  to  the  patients,  who  were  warned  of  possibilities,  but 
such  as  yet  have  not  been  reported. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA  627 

A  chronic  abscess  may  discharge  into  the  maxillary  sinus  for  a 
long  period  before  being  discovered,  unless  the  pus  accumulation  be 
extensive,  when  it  escapes  from  the  antrum  into  the  cavity  of  the 
nose,  discharging  b}'^  one  side.  Smaller  accumulations  of  pus  find 
exit  in  the  recumbent  position,  and  attention  is  called  to  one  antrum 
as  the  seat  of  affection  by  noting  that  in  the  morning  pus  appears 
at  but  one  nostril.  The  discharges  from  purulent  nasal  catarrh 
appear  upon  both  sides. 

Fig.  580 


Two  artificial  roots  in  drilled  sockets.     Greenfield.     (See  text.) 

A  more  common  history  of  antral  empyema  is  the  patient's  com- 
plaint of  dull,  heavy  pains  and  uneasiness  over  one  side  of  the  face, 
and  an  offensive  odor,  which  may  not  be  evident  to  the  operator. 
High  transillumination  of  the  tissues  about  the  mouth  and  through 
the  cheek,  by  means  of  the  electric  mouth  lamp  of  20  volts  capacity, 
the  patient  being  in  a  dark  room,  may  reveal  an  opacity  on  one  or 
perhaps  both  sides,  indicating  the  presence  of  fluid  in  the  antrum. 
A  clear  pinkish  transillumination  is  a  sign  of  health.  Tumors  in  the 
antrum  entirely  obstruct  the  light.  Examination  of  the  posterior 
teeth  will  show  one  of  them  to  be  pulpless,  if  the  cause  lies  in  apical 
abscess.  If  such  a  tooth  be  extracted,  a  profuse  flow  of  pus  may 
follow,  and  a  probe  may  be  passed  through  an  alveolus  directly  into 
the  antrum. 

The  diagnosis  may  be  assisted  by  a-rays,  both  antra  being  radio- 


628     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

graphed  for  comparison.  Raper^  states  that  the  shadow  does  not 
actually  demonstrate  the  presence  of  pusi  but  that  something  abnor- 
mal exists  whether  pus  or  a  soft  tumorous  growth,  the  appearance 
being  the  same.     It,  however,  locates  the  disease,  whether  in  the 

Fig.  581 


A,  antrum  with  pus  in  it.    B,  healthy  antrum.    (Radiograph  by  Carmen  of  St.  Louis.) 
Courtesy  of  Dr.  Howard  R.  Roper. 


antrum  or  other  sinuses.     The  presence  of  opaque  foreign  bodies, 
as  a  piece  of  tooth  root  causing  disease,  is  shown  by  skiagraphy. 
Although  extraction  is  the  usual  surgical  relief,  dental  conserv- 
atism rebels  against  the  immediate  condemnation  of  the  offending 

1  Items  of  Interest,  July,  1912. 


CHRONIC  APICAL  ABSCESS  WITH  FISTULA 


629 


Fig.  582 


tooth.  Efforts  at  curing  the  antral  condition  through  the  pulp 
canal  are  well-nigh  hopeless — the  antrum  is  entered  at  some  other 
point.  The  tooth  is  treated  as  any  infecting  root;  is  sterilized  and 
filled.  The  most  certain  spot  of 
entry  to  the  antrum  is  about  one- 
quarter  inch  above  the  buccal  roots 
of  the  upper  first  molar  or  between 
the  roots  of  the  first  and  second 
molar.  The  part,  or  the  patient, 
is  anesthetized,  and  the  soft  tis- 
sues incised  or  a  section  removed 
by  means  of  a  tubular  knife;  a 
drill  or  trephine  at  least  one-eighth 
inch  in  diameter,  driven  rapidly,  is 
passed  upward,  backward,  and  in- 
ward, piercing  the  thin  shell  of  the 
antrum  at  this  point.  The  opening 
is  made  of  convenient  size  to  admit 

of  thorough  exploration.  The  nozzle  of  an  atomizer  or  syringe,  filled 
with  a  mild  antiseptic  solution,  is  passed  into  the  antrum  and  the 
cavity  is  freely  sprayed.  A  probe  or  the  finger  is  passed  into  the  cavity 
and  an  exploration  made  to  detect  the  presence  of  any  dead  bone  or 


Emypema  of  antrum  due  to 
abscess  upon  root  of  bicuspid  tooth. 
(Radiograph  by  Price.) 


Fig.  583 


Fig.  584 


Scar  caused  by  alveolar  abscess  dis- 
charging on  the  face.     (Black.) 


Operation  for  the  remedy  of  scar  on  the  face 
caused  by  alveolar  abscess.     (Black.) 


bony  septi,  which,  if  found,  must  be  removed,  the  cavity  of  entrance 
being  enlarged  to  permit  their  removal.  The  antrum  is  then  packed 
with  gauze  impregnated  with  iodoform,  etc.     After  a  few  days  the 


630     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

cavity  is  sprayed  about  every  other  day  with  very  dilute,  warm 
Dobell's  solution,  Lugol's  solution,  or  sterile  ocean  water.  (For  further 
information  see  works  on  Oral  Surgery.)  The  opening  either  heals 
of  itself  or  may  be  made  to  do  so  by  the  use  of  caustics  or  stitching 
the  parts. 

Unless  necrosis  of  bone  occur,  cases  of  fistula  opening  upon  the 
face  or  neck  may  be  healed  by  the  ordinary  methods  of  canal  treat- 
ment, carried  out  with  extraordinary  care  to  accomplish  the  irriga- 
tion of  the  fistula,  or  at  least  sterilize  the  apical  tissue.  The  scar 
formation  is  less  than  when  extraction  is  practised  for  the  removal 
of  the  cause.  If  the  fistula  be  indolent,  the  granulations  may  be 
stimulated  by  means  of  an  injection  of  10  per  cent,  silver  nitrate 
solution.  If  the  fistula  obstinately  refuse  to  heal,  the  tooth  should 
be  extracted  and  necrosed  bone,  if  any  be  present,  surgically  removed, 
though  amputation  of  the  root  apex  may  be  tried. 

Flagg^  suggested,  as  a  means  of  lessening  scar  formation,  that  a 
seton  be  passed  through  the  external  fistula  into  the  mouth,  and  that 
it  be  gradually  drawn  into  the  mouth  as  the  external  fistula  heals, 
after  which  the  tooth  is  to  be  extracted  if  otherwise  incurable. 

In  fistulse  discharging  upon  the  face  the  formation  of  scar  tissue 
may  bind  the  tissue  of  the  cheek  tight  to  the  bone.  When  this 
occurs  beneath  the  tip  of  the  chin,  the  scar,  after  healing,  usually 
resembles  a  dimple,  and  calls  for  no  interference.  The  scar  and 
binding  down  along  the  border  of  the  inferior  maxilla,  or  beneath 
the  malar  bone  in  the  upper  maxilla,  may  produce  deformity  calling 
for  remedy  (Figs.  583  and  584).  Black's  operation  is  to  be  performed 
to  lessen  the  deformity,  for  its  complete  correction  is  not  practicable. 
A  finger  placed  in  the  mouth  draws  the  cheek  away  from  the  alveolar 
wall,  when  the  exact  position  of  the  cord  of  attachment  is  discovered. 
A  tenotome  knife  is  passed  into  the  tissues,  dividing  the  band  of 
attachment;  a  long  pin  is  passed  through  the  most  depressed  portion 
of  the  scar,  its  centre,  the  long  ends  of  the  pin  resting  upon  the 
face;  strips  of  adhesive  plaster  laid  upon  the  skin  under  the  head 
and  point  of  the  pin  will  prevent  the  latter  sinking  into  the  soft 
tissues.  The  pin  is  retained  for  several  days,  until  the  cut  in  the 
mouth  heals.  The  principle  involved  is  the  supplying  of  a  new 
section  of  scar  tissue  which,  while  it  shrinks,  makes  the  total  length 
of  the  cord  greater,  hence  less  binding. 

Systemic  Complications. — The  cachectic,  debilitated,  anemic,  tuber- 
culous, and  syphilitic  are  liable  to  extensive  pus  formation,  which 
enlarges  the  cavity  unduly  and  may  involve  the   roots   of  other 

1  Lectures  on  Dental  Therapeutics. 


CHRONIC  BLIND  APICAL  ABSCESS  631 

teeth  or  even  cause  devitalization  of  their  pulps,  which  aids  in  the 
continuance  of  the  abscess  by  adding  a  fresh  cause. 

In  such  cases  all  the  dead  pulps  should  be  removed  after  careful 
diagnosis,  and  the  patient  should  be  instructed  in  the  use  of  a  Sub. 
Q.  syringe  and  a  mild  antiseptic,  the  object  being  to  keep  the  depend- 
ent parts  free  of  pus  and  allow  granulations  to  form  rather  than 
be  constantly  broken  down.  In  such  cases  hydrogen  dioxid  should 
be  avoided  as  it  may  force  undestroyed  bacteria  into  remote  parts. 

In  addition,  such  systemic  medication  or  remedial  measures  as 
will  raise  the  recuperative  and  resistant  powers  of  the  tissues  should 
be  employed. 

If  very  persistent,  a  vaccine  may  be  employed,  after  the  method 
of  Wright,  to  raise  the  opsonic  index.  (See  p.  63.)  The  direct  results 
of  infection,  toxemic  and  septicemic,  have  already  been  considered. 
Grieves  contends  that  many  root  ends  remain  necrotic  and  develop 
blind  abscesses  and  their  sequelae  (which  see). 

Chronic  Blind  Apical  Abscess. — A  true  blind  abscess  is  one  with- 
out a  point  of  discharge.  It  is  a  result  of  septic  contamination 
from  root  canals,  a  condition  in  which  bacteria  in  unfilled  root 
apices  or  in  the  interspaces  between  a  root  filling  and  the  canal 
wall  find  their  way  into  the  fiuid  entering  such  a  space  and  produce 
putrefaction — a  condition  practically  analogous  to  moist  gangrene 
of  the  pulp;  or  else  bacteria  in  the  blood  arising  from  some  other 
source,  dental,  tonsillar,  or  other  focus,  or  entering  to  form  a  general 
blood  infection,  enter  an  apical  region  previously  weakened  as  by 
pulp  removal,  apical  irritation  by  root  canal  filling,  a  previous  abscess, 
etc.,  and  develops  a  chronic  apical  abscess. 

An  apical  abscess  is  formed  and  the  apical  tissue  acts  as  a  fibro- 
vascular  envelope  or  sac.  Under  the  pus  pressure  and  the  pumping 
force  of  masticatory  movement,  absorption  of  toxins  and  pus  germs 
by  way  of  the  lymphatics  occurs.  The  lymphatic  glands  may  be 
involved;  a  systemic  infection  occurs. 

HartzelP  states  that  Rosenow  has  shown  that  streptococci 
found  in  the  mouth  and  tonsils  can  be  made  under  suitable  condi- 
tions to  change  into  typical  and  encapsulated  lanceolate  pneumococci; 
or  under  other  cultural  conditions  to  produce  organisms  which 
locate  in  the  joints,  causing  arthritis  deformans;  and  under  still 
different  cultural  conditions  to  produce  Streptococcus  viridans  which 
is  the  common  organism  in  heart-valve  lesions,  and  under  still  other 
cultural  conditions  to  become  capable  of  causing  ulcers  of  the 
stomach  and  bowels. 

1  Journal  of  the  Allied  Societies,  June,  1914 


632     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

In  animals  Rosenow  has  experimentally  brought  about  heart 
lesions,  from  the  bacteria  in  these  heart  lesions  has  caused  ulcer  of 
the  stomach.  From  the  bacteria  there  he  has  caused  joint  affections. 
From  these  he  has  produced  typical  pneumonia,  and  from  the  lung 
removed  the  original  strain  of  organism  which  was  also  tested  out 
along  the  series. 

Hartzell  has  observed  that  when  abscesses  or  pyorrhea  pockets 
are  freely  communicating  with  air  streptococci  are  most  often  non- 
hemolytic. In  deep  but  active  abscesses  they  are  hemolytic.  In 
long  standing  and  blind  abscesses  they  are  non-hemolytic  owing 
to  encapsulation  and  the  depressive  activity  of  their  own  metabolic 
products. 

Hartzell,  in  support  of  transmutation  of  bacteria,  cites  Larsen 
as  causing  the  fusibacillus  to  develop  a  typical  spirillum  and  again 
relapse  into  the  fusiform  bacillus.  (This  may  account  for  Vincent's 
fusibacilH  and  spirilli  found  in  conjunction  in  Vincent's  angina.)- 

He  quotes  Schottmiiller  as  isolating  streptococcus  mucosus  from 
the  lesions  of  parametritis,  meningitis,  and  phlebitis  and  shows  its 
biological  characteristics  as  allied  to  those  of  pneumococcus.  By 
experiments  carefully  conducted  to  exclude  oral  bacteria  from  septic 
root  ends  clipped  into  media,  Hartzell  developed  streptococci  which, 
entering  the  blood  with  their  toxins,  travel  to  distant  points  and 
produce  systemic  toxemia  and  local  manifestations.  It  seems, 
therefore,  reasonably  clear  that  ordinarily  harmless  bacteria,  as 
S.  viridans  and  the  fusibacillus,  may  transmute  into  virulent  ones 
by  a  change  in  cultural  conditions. 

According  to  Grieves^  the  following  distant  manifestations  may 
occur,  as  the  result  of  combined  ingestion  and  absorption  of  pyogenic 
cocci  and  the  production  of  a  septicemia  and  toxemia: 

1.  Upon  the  muscles,  causing  myositis. 

2.  Upon  the  joints,  causing  arthritis,  synovitis,  etc. 

3.  Upon  the  blood,  causing  septic  and  pernicious  anemia  and 
endocarditis  or  pleurisy. 

4.  Upon  the  glands,  causing  lymphadenitis. 

5.  Upon  the  nervous  system,  causing  toxic  neuritis  and  degenera- 
tion. 

6.  Upon  the  organs  of  excretion,  causing  skin  rashes  and  nephritis. 

7.  Upon  the  gastro-intestinal  tract,  causing  septic  gastritis,  enter- 
itis, cholecystitis,  appendicitis,  colitis,  etc. 

In  the  kidney  lesions,  Hartzell  notes  albuminuria  and  casts  in 
quantity,  lessening  as  the  local  foci  of  pus  formations  are  removed.^ 

1  Dental  Cosmos,  May,  1914,  p.  568. 

2  Journal  of  Allied  Societies,  June,  1914. 


BONE  INFECTION  ASSOCIATED  WITH  DENTAL  LESIONS     633 

The  symptom-complex^  is  mainly  an  anemic,  pasty  complexion, 
malaise,  loss  of  appetite,  debility,  night  sweats,  loss  of  weight,  low 
fever  (100°),  or  subnormal  temperature,  which,  together  with  the 
local  inflammation  (muscles,  joints,  etc.),  should  lead  to  dental 
examination  by  skiagraphy  for  obscure  conditions  as  blind  apical 
abscess  or  the  investigation  of  septic  conditions  under  crowns, 
bridges,  etc.  (as  septic  gingivitis,  septic  spaces  under  crown  bands  or 
in  the  cement,  gangrenous  tooth  pulps,  pyorrhea  alveolaris,  fistulse 
leading  to  chronic  abscess,  tonsillar  or  sinus  infection.  In  short, 
any  source  of  sepsis,  some  of  w  hich  may  require  the  services  of  other 
specialists. 

The  abscesses  are  within  the  bone  of  the  jaw  while  the  dental 
symptoms  may  not  be  noticeable,  though  the  tooth  may  be  slightly 
tender  and  there  may  be  tenderness  upon  pressure  over  the  apical 
region.  There  may  be  pain  about  the  eyes  or  in  the  back  of  the  head 
or  neck.  The  postcervical  glands  may  be  enlarged.  The  fact 
that  teeth  have  apparently  been  attended  to  is  no  warrant  that 
septic  conditions  are  not  present,  these  conditions  embracing  any 
form  of  gingivitis  or  of  pericemental  infection,  including  pyorrhea. 
a  blind  abscess  may  at  any  time  become  acute,  and  finally  establish 
a  fistula,  sometimes  irregularly  and  without  much  pain. 


BONE  INFECTION  ASSOCIATED  WITH  DENTAL  LESIONS. 

During  the  course  of  acute  and  chronic  abscess  the  bone-marrow 
becomes  inflamed  by  the  pyogenic  organisms  and  is  broken  down 
into  pus.  The  condition  may  continue  after  extraction  for  apical 
abscess  in  the  second  stage,  or  if  necrotic  bone  result  in  advanced 
pyorrhea.  It  may  also  occur  from  the  bruising  of  the  periosteal 
lining  of  the  alveolus  as  the  result  of  extraction  of  a  hyper- 
cementosed  root,  or  from  a  bruise  induced  by  forcible  use  of 
forceps  in  the  removal  of  deeply  seated  roots. 

The  walls  of  the  alveolus  become  infected  by  pyogenic  organisms, 
among  which  the  Diplococcus  pneumonise  figures  prominently. 

The  leaving  of  cotton  tampons,  placed  as  vehicles  for  pain-relieving 
agents,  for  an  undue  length  of  time  also  invites  infection. 

If  during  extraction  the  alveolar  margins  be  lacerated,  and  espe- 
cially if  the  bone  be  uncovered  by  clot,  or  the  clot  fail  by  solution, 
it  also  becomes  infected  and  ulcerated,  as  shown  by  its  suppurating 
and  highly  irritable  surface;  later  the  surface  becomes  insensitive, 

»  Dental  Cosmos,  May,  1914,  p.  569. 


634     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

indicating  superficial  necrosis,  which  may  become  progressively 
deeper.  The  clot  seems  to  fail  at  times  after  extraction  with  anes- 
thetics containing  adrenalin  or  suprarenin.  In  some  cases  the  socket 
may  be  free  of  blood  for  several  minutes  after  extraction.  Ragged 
gum  margins  may  become  gangrenous,  although  sometimes  not. 
After  extraction  any  loose  margin  of  gum  or  rough  edges  of  process 
should  be  trimmed  up. 

Symptoms. — The  symptoms  are  those  of  local" inflammation  with- 
out necessarily  much  swelling  of  contiguous  tissues,  such  as  occurs 
in  acute  abscess.  Some  circumscribed  swelling  may  occur,  indicating 
an  abscess  in  association  with  it,  or  a  diffuse  swelling,  indicating 
inflammation  of  contiguous  tissue.  The  orifice  may  appear  as 
though  normal,  but  close  examination  demonstrates  a  sinus  leading 
to  ulcerated  or  necrosed  bone.  If  due  to  an  acute  abscess  in  the 
second  stage,  the  symptoms  of  that  condition  may  continue.  As  a 
rule,  the  patient  presents  within  a  week  of  the  date  of  extraction, 
complaining  of  pain. 

In  the  majority  of  cases  the  pain  is  of  a  deep,  boring,  continuous 
character.  Reflex  pains  are  also  produced  about  the  face.  Much 
debility  is  caused  by  the  wearing  character  of  the  pain,  the  loss  of 
sleep  and  appetite,  and  probably  also  because  of  absorption  of 
toxins.  The  gum  margins  are  perhaps  sloughing;  the  bone  may  be 
exposed  and  exquisitely  painful  to  touch,  or  it  may  be  necrotic  and 
insensitive  superficially.     The  case  is  one  termed  "dry  socket." 

Cases  of  general  septicemic  or  pyemic  infection  from  this  source 
have  been  recorded. 

Treatment. — The  mouth  and,  in  so  far  as  possible,  the  inflamed 
part  must  be  sterilized.  Probably  mercuric  chlorid  in  hydrogen 
dioxid  (1  to  1000)  will  answer  best.  If  the  solution  be  used  hot, 
whether  it  be  mercurialized  or  not,  the  pain  is  much  relieved. 

An  injection  of  a  1  or  2  per  cent,  solution  of  cocain  into  the  healthy 
tissue  overlying  the  alveolus  will  assist  in  alleviating  the  acute  pain 
and  partly  anesthetize  the  parts.  All  sloughing  gum  should  be  cut 
away.  Exposed  bone  should  be  anesthetized  by  strong  cocain  solu- 
tions if  painful  to  touch,  or  the  patient  should  be  anesthetized  if 
necessary.  Whether  acutely  inflamed  or  necrotic,  the  bone  should 
be  cut  away  with  large  sterile  burs  until  healthy  tissue  is  reached. 
After  washing  out  the  debris  and  further  sterilization  a  clot  is  to 
be  induced  by  curetting  if  necessary.  The  mouth  is  to  be  kept 
sterilized  and,  the  patient  is  to  be  seen  daily  for  a  repetition  of  the 
curetting  if  the  clot  fail,  or  the  alveolus  may  be  gently  packed  with 
cotton  saturated  with  balsam  of  Peru  alone  or  with  castor  oil,  equal 
parts,  as  a  stimulant.    In  ordinary  cases  one  or  two  local  treatments 


EXTENSIVE  NECROSIS  635 

will  be  effective,  but  the  tonic,  antiseptic,  systemic  medication 
recommended  under  the  heading  of  acute  apical  abscess  is  advised. 

As  a  stimulant  for  granulating  sockets,  tincture  of  iodine  diluted 
with  equal  parts  of  tincture  of  aconite  or  alcohol  is  valuable  because 
of  its  irritant  and  disinfectant  qualities.  The  socket  is  wiped  with 
it  daily. 

If  the  infection  be  of  aggravated  character,  precautions  in  the  form 
of  suitable  systemic  medication  should  be  taken  against  a  possible 
septicemia.     (See  p.  604.) 

If  the  patient  be  not  willing,  or  is  unable,  to  bear  this  operation  at 
the  first  visit  because  of  the  demoralization  produced  by  the  pain, 
an  alternative  proceeding  may  be  adopted.  A  pellet  of  cotton  wet 
with  campho-phenique  should  be  rolled  in  powdered  orthoform  and 
introduced  into  the  socket  after  sterilization  with  iodine,  or  a  stiff 
mass  made  from  orthoform,  zinc  oxid,  and  vaselin  may  be  packed 
into  the  alveolus  as  an  antiseptic  and  anesthethic.  (Jack.^)  Tri- 
chloracetic acid  in  saturated  solution,  or  silver  nitrate,  or  aromatic 
sulphuric  acid  may  be  used  as  a  special  stimulant  and  the  balsam 
packing  renewed.  The  repetition  of  this  after  five  to  eight  hours 
will  afford  marked  relief.  Later  the  radical  operation  may  be  per- 
formed if  granulation  does  not  set  in.  The  introduction  of  cotton 
or  gauze  dressings  into  the  alveoli  for  relief  of  pain  immediately 
following  extraction  is  to  be  done  only  with  extreme  care  and  for 
short  periods,  as  such  dressings  are  apt  to  be  left  in  place  by 
patients,  and,  becoming  septic,  act  as  causes  of  sepsis  of  the  alveolar 
process.  It  is  better  to  induce  a  clot  if  the  removal  of  the  cotton 
is  not  followed  by  hemorrhage.  While  alveoli  will  fill  with  granula- 
tions in  the  absence  of  a  clot  filling  them,  such  a  clot  seems  to  be 
the  best  protection  against  sepsis  and  a  depressed  scar  tissue.  In 
some  of  these  cases  portions  of  bone  may  exfoliate.  In  one  obsti- 
nate case  the  capsule  of  bone  surrounding  the  apex  of  the  alveolus 
came  away. 


EXTENSIVE  NECROSIS  ASSOCIATED  WITH  CHRONIC 
ALVEOLODENTAL  ABSCESS. 

The  illustration  (Fig.  585)  is  that  of  a  case  of  necrosis  with  two 
external  pus  sinuses  along  the  lower  border  of  the  mandible,  associated 
with  great  pain  on  recumbency,  rise  and  fall  of  body  temperature, 
and  occurrence  of  stupor  and  coma.    The  operation  consisted  of  ex- 

1  International  Dental  Journal,  1905. 


636     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

traction  of  the  cuspid  and  first  bicuspid,  removal  of  the  sequestrum, 
curettement  of  bone,  and  drainage.^ 

Fig.  585 


The  white  Hne  is  artificial  and  shows  the  extent  of  the  sequestrum  (see  text). 
(Skiagraph  by  Raper.) 

Every  chronic  alveolodental  abscess  carries  with  it  the  danger  of 
bone  compHcation.  It  has  been  shown  that  in  bone  infection  the 
organisms  are  highly  virulent.  Fortunately  in  most  cases  the  involve- 
ment is-  sligh't  and  the  parts  care  for  themselves  when  the  cause  is 
removed.  In  more  aggravated  cases,  either  caries  or  necrosis  of  the 
bone  may  follow.  Pus  is  formed  at  the  expense  of  the  parts,  and 
sometimes  infiltrates  the  surrounding  soft  and  the  hard  parts,  caus- 
ing the  loosening  of  teeth.  This  may  occur  even  though  the  causal 
tooth  be  extracted.  In  caries  the  pus  escapes  by  several  fistulse 
and  examination  leads  to  porous  dead  bone.  In  necrosis  there 
is  circumvallation  of  a  portion  or  portions  of  bone,  and  finally  one 
or  more  sequestra  are  loosened,  and  later,  in  part,  liquefied.  The 
remainder  gradually  works  out  of  the  fistula  as  one  large  or  numerous 
small  pieces.  The  patient  may  be  much  debilitated.  In  syphilitic 
or  strumous  cases  an  otherwise  simple  case  may  positively  refuse 
to  heal  until  the  physical  condition  is  improved  by  antisyphilitic 

1  Practice  of  Dr.  Gilmer,  description  by  Howard  R.  Raper,  Items  of  Interest,  July, 
1912. 


SEPTIC  PERFORATION  637 

or  tonic  treatment.  Surprising  recoveries  of  extensively  necrotic 
parts  occur  if  the  patient  be  brought  into  good  physical  condition, 
and  the  parts  are  antiseptically  treated,  the  thorough  loosening  of 
the  sequestra  being  awaited.  By  this  means  teeth  have  been  retained 
in  place  and  covered  with  new  tissue,  which  operation  would  have 
exposed  or  removed.  The  determination  of  the  point  at  which  oper- 
ative interference  is  desirable  must  depend  upon  the  particular 
case  and  the  amount  of  deformity  likely  to  result  from  the  operation. 
In  some  marked  cases  with  toxemia,  drainage  must  be  obtained 
surgically,  even  if  extreme  operation  be  necessary. 

Honl  and  Bukovsky  are  credited  with  the  successful  treatment 
of  bad  chronic  suppurations  by  means  of  local  applications  of 
pyocyaneoprotein. 

Jensesky^  so  treated  a  case  of  six  months'  standing,  incurable  by 
ordinary  antiseptic  and  systemic  treatment,  and  obtained  remarkable 
results.     Vaccine  therapy  is  also  useful. 

Syphilitic  intoxication  or  that  of  scarlet  fever  may  cause  a  necrosis 
of  alveolar  bone,  as  may  mercury.  (See  p.  231.)  The  extent  to 
which  the  teeth  or  oral  infection  act  as  active  exciting  causes  depends 
upon  the  condition  present. 

SEPTIC  APICAL  PERICEMENTITIS  COMPLICATED  BY 
PERFORATION. 

In  the  treatment  of  root  canals  the  required  mechanical  work 
sometimes  results  in  (1)  the  passage  of  the  drill  through  the  apical 
foramen,  enlarging  it;  (2)  through  the  side  of  the  root,  causing  a 
perforation. 

In  the  first  variety  the  complication  chiefly  concerns  the  root 
filling,  which  is  to  be  conducted  after  sterilization  upon  the  same 
plan  as  for  filling  an  incomplete  foramen.     (See  p.  555.) 

If  a  lateral  perforation  be  made  near  the  root  apex,  it  may  be 
filled  after  sterilization  with  a  cone  similarly  applied,  but  made 
bevelled  at  the  end,  or  a  bit  of  aseptic  sponge  may  be  introduced 
against  the  tissue  for  a  base  and  be  covered  by  oxychlorid  of  zinc. 
The  packing  of  a  fairly  stiff  mass  of  zinc  oxychlorid  into  the  root 
and  through  the  perforation  into  the  fistula  has  caused  the  healing 
of  several  obstinate  cases  continually  weeping  pus  or  serum.  The 
moisture,  if  slight,  rather  aids  the  adaptation  of  the  cement.  The 
same  treatment  used  with  greater  care  is  useful  in  chronic  abscesses 
without  fistula.     It  is  well  to  fill  only  the  apical  portions  of  canals  in 

1  Dental  Cosmos,  1901. 


638     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

either  case,  so  that  any  removal  for  another  trial  may  not  be  too 
difficult;  the  later  filling  of  the  coronal  portion  of  the  canal  is  very 
simple.  The  use  of  a  stiff  paste  of  zinc  oxid  and  eugenol  or  even 
oxyphosphate  of  copper  in  the  same  manner  is  useful.  If  possible, 
it  is  well  to  irrigate  the  fistula  with  water  to  remove  any  excess, 
though  if  left  it  usually  works  out  of  the  fistula,  which  later  heals 
or  not,  as  the  case  may  be.  If  septic  conditions  persist,  the  root 
end  must  be  amputated,  or  the  tooth  extracted,  prepared,  and 
replanted.  If  made  in  the  middle  third  of  the  root,  the  canal  must 
be  sought  for  and  treated  as  usual  beyond  the  perforation,  which  is 
then  separately  treated  with  a  gutta-percha  cone,  or  a  plaque  of 
gutta-percha  may  be  laid  over  the  perforation  and  antiseptic  cements 
or  copper  amalgam  used  to  secure  it  in  position.  Extraction  and 
replantation  may  be  resorted  to,  but  amputation  does  not  serve 
so  well,  as  the  root  leverage  is  lost  and  the  tooth  may  loosen.     In  a 

Fig.  586  Fig.  587 


Skiagraph  of  crowned  curved  root,  with  Showing  the  relations  of  an  abscess 

perforation   and    protruding    root    filling  upon  a  temporary  tooth,  with  the  crown 

near  apical   foramen.     With  septic  con-  of  a  developing  permanent  tooth  under- 

ditions,  would  require  root  amputation.  lying  it. 
(Price.i) 

favorable  case,  after  canal  exploration,  a  tapering  probe  may  be 
passed  into  the  canal  and  copper  amalgam  gently  tamped  about  it 
and  against  the  perforation;  the  probe  is  then  withdrawn,  leaving 
a  central  canal,  which  is  later  treated.  Gird  wood  has  reported  good 
results  from  the  use  of  copper  amalgam,  which,  in  this  connection, 
the  writer  can  confirm.  In  a  few  cases  the  fistula  has  been  packed 
open  and  the  perforation  filled  with  amalgam  through  the  sinus. 
The  cases  are  mostly  successful,  but  in  one  case  healing  did  not 
occur  until  treatment  after  filling  was  suspended  for  several  months. 
Chronic  Septic  Pericementitis  in  the  Temporary  Teeth. — Any  of  the 
chronic  septic  conditions  described  may  occur  upon  the  temporary 
teeth.     The  presence  of  resorption  and   of  the  permanent  crown 

1  Items  of  Interest,  1901. 


APICAL  PERICEMENTITIS  IN   TEMPORARY  TEETH       639 

usually  confines  the  inflammation  to  a  point  lower  in  the  alveolar 
process  than  in  the  case  of  permanent  teeth.  The  loose  character 
of  the  structure  causes  the  ulceration  to  occupy  a  larger  area,  and 
the  parts  in  chronic  inflammation  look  more  angry,  but  are  fairly 
well  tolerated.  The  treatment  is  practically  the  same  for  the  curable 
cases;  the  others  should  be  extracted.  The  root  canals  when  treated 
should  be  filled  with  absorbable  materials,  such  as  paraffin  or  wax 
combined  with  aristol.  Buckley  recommends,  as  a  canal  filling  in 
these  cases,  the  use  of  a  stiff  mixture  of  calcium  phosphate  and 
formocresol  (formalin,  1  part;  cresol,  1  or  2  parts),  to  be  packed  into 
the  pulp  chamber  and  zinc  phosphate  quickly  flowed  over  it;  the 
cavity  to  be  filled  later. 

Johnson^  suggests  that  a  eucalyptol  solution  of  gutta-percha  (see 
p.  551)  be  pumped  into  the  canals  and  pressure  exerted  with  tempo- 
rary stopping  until  the  solution  appears  at  the  fistula.  The  tem- 
porary stopping  that  does  not  interfere  \^ith  filling  integrity  should 
be  left. 

Chronic  Septic  Apical  Pericementitis  (Non-purulent). — Continued 
apical  inflammation  of  a  low  grade  probably  is  a  condition  analogous 
to  blind  chronic  apical  abscess  or  the  infection  leading  thereto. 

Cause  and  Pathology.^The  cause  consists  of  unremoved  gan- 
grenous pulp  tissue,  septic  serous  collections  in  canal  apices  or 
about  imperfect  root  fillings,  or  septic  material  in  the  root  tubuli, 
all  much  the  same  in  character.  A  very  common  cause  is  an  other- 
wise good  root  filling  which  has  failed  to  fill  the  apical  portion  of  a 
curved  fine  or  even  well-opened  root.  While  in  skilful  hands  gutta- 
percha points  and  oxychlorid  of  zinc  usually  reach  their  apical 
destination,  the  editor  has  met  unfilled  apical  canals  after  good 
operators  as  the  most  common  of  operative  errors. 

An  imperfectly  filled  perforation  may  cause  a  similar  condition, 
which,  however,  the  .r-rays  should  determine. 

Albuminous  fluid  may  enter  the  canal  via  the  apical  foramen,  and, 
becoming  infected,  putrefaction  ensues.  The  source  of  infection 
may  possibly  be  ria  the  blood,  but  leaking  crown  and  root  fillings 
more  probably  permit  bacteria  to  enter  from  the  mouth.  The 
more  or  less  constant  result  of  filling  roots  with  cotton  permeated 
with  evanescent  materials  only  is  evidence  of  this.  The  cotton 
absorbs  fluid  either  from  about  leaky  fihings,  too  often  placed  in 
contact  with  it,  or  else  from  the  apical  tissues;  infection  readily 
occurs  and  a  highly  odorous  cotton  is  removed  because  of  the  apical 
irritation.     When   the   cotton   is   well   placed   and   confined   under 

1  Dental  Cosmos,  1899. 


640     DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

tight-sealing  materials  to  the  apical  half  of    the  root  canal,  this 
result  is  long  delayed  in  many  cases.     Portions  of  gangrenous  pulps 


Fig.  588 


Dentin  from  the  root  of  an  abscessed 
tooth,  showing  the  penetration  of  cocci  to 
a  depth  of  about  yV  mm.  (^io  in.);  the 
side  a  to  b  bordered  upon  the  canal- 
X  1000.     (Miller.) 


ll* 


Sector  of  a  cross-section  from  a  dis- 
eased root:  a,  cementum;  b,  stratum 
granulosum;  c,  very  narrow  and  finely 
branched  tubules;  d,  penetration  of 
bacteria  into  tubules.  X  150. 
(Miller.) 

1  Dental  Cosmos,  1899. 


remaining  in  canals  may  likewise 
become  infected.  Extra  and  un- 
treated canals  are  frequently  causes. 

Miller^  has  shown  that  root 
tubules  are  infected  only  for  a 
short  distance  at  their  canal  ends, 
so  that  infection  from  the  perice- 
mentum via  the  cementum  and 
dentinal  tubules  is  highly  improb- 
able (Fig.  559).  The  putrefaction 
produces  gases,  and  these  exuding 
slowly  produce  the  irritation.  If 
pyogenic  organisms  be  present, 
apical  abscess  may  at  any  time 
supervene. 

Mayrhofer^  has  shown  that  even 
formocresol    fails    to    sterilize    all 

2  Items  of  Interest,  March,  1910. 


CHRONIC  SEPTIC  NON-PURULENT  PERICEMENTITIS    641 

tubuli,  so  that  bacteria,  especially  streptococci,  grow  back  into  the 
canal.  If  the  canal  filling  be  imperfect  it  is  obvious  that  apical 
infection  may  arise. 

Symptoms. — Subacute  inflammation  of  apical  tissue  being  present, 
the  symptoms  of  this  condition  are  tenderness  upon  decided  pressure 
or  upon  percussion;  the  response  may  only  be  elicited  by  pressure 
or  percussion  in  one  direction.  The  tooth  gives  a  dull  note  upon 
percussion,  and  is  usually  looser  than  its  neighbors.  The  red  line  of 
the  gum  extends  farther  toward  the  gum  margin  than  normal — quite 
to  it  in  some  cases.     There  is  apt  to  be  a  response  to  heat. 

The  patient  is  apt  to  avoid  the  tooth  in  mastication.  In  some 
cases  acute  reflex  pains  in  other  teeth  may  precede  an  outbreak  of 
acute  purulent  pericementitis,  a  frequent  sequel  to  this  condition. 
There  are  also  evidences  of  previous  devitalization  of  the  pulp  in 
opacity,  lack  of  response  to  tests  for  vitality,  etc.  At  times  a  history 
of  previous  canal  treatment  may  be  obtained  or  the  evidences  of  an 
attempt  at  canal  filling  may  be  seen  upon  opening  the  tooth.  The 
systemic  symptoms  if  any  are  those  mentioned  under  chronic  apical 
abscess. 

Diagnosis.^ — The  condition  requires  careful  differentiation  from  (1) 
non-septic  apical  pericementitis  due  to  traumatism  or  malocclusion 
or  to  a  perforation  imperfectly  filled;  (2)  pericemental  abscess  in 
the  early  stage;  (3)  abscess  of  the  pulp  in  the  later  stages.  In  nearly 
all  these  cases  the  pulp  may  be  vital.  Being  itself  only  subsequent 
to  death  of  the  pulp,  tests  for  vitality  are  made.  (See  p.  563.) 
If  pulp  death  be  indicated  by  the  tests,  the  pulp  canal  is  explored, 
and,  if  found,  treated  and  filled;  a  septic  condition  about  or  beyond 
the  same  is  looked  for. 

There  is  great  disadvantage  in  a  large  apical  opening,  particularly 
in  the  dressing  and  root-filling  operation. 

Treatment. — The  condition  being  analogous  to  that  of  moist 
gangrene,  or  blind  apical  abscess,  the  treatment  is  the  same.  Before 
it  can  be  applied  the  root  canals  should  be  opened,  and  to  accomplish 
this  all  root  fillings  involved  require  removal.  If  an  extra  canal  be 
found  after  apparently  conscientious  work  has  been  done,  this 
should  receive  attention  before  removing  root  fillings. 

The  bulk  of  gutta-percha  root  fillings  are  best  drilled  out  with 
Downie  broaches  revolved  in  the  engine  hand-piece  or  by  hand, 
eucalyptol  being  used  to  soften  or  dissolve  the  gutta-percha. 

All  cement  fillings  are  removed  by  a  drill  so  far  as  can  be  safely 

done,  dryness  being  a  great  aid  in  locating  the  cement  in  the  canal. 

When  the  danger  of  perforation  arises,  a  stiff  Swiss  broach  or  a  fine 

Downie  broach  may  be  rubbed  down  to  a  drill  edge  and  used  as  a 

41 


642      DISEASE  OF  PERICEMENTUM  BEGINNING  AT  APEX 

tamp  drill.     Sulphuric  acid  in  50  per  cent,  solution  or  aqua  ammonia 
aid  by  dissolving  the  cement. 

The  object  sought  for  is  an  unfilled  canal  lumen,  which,  when 
found,  is  readily  recognized  by  the  ease  of  penetration  with  the 
broach  and  the  absence  of  sensation  until  the  apical  tissue  is  reached. 
The  fact  that  the  sides  of  the  root  canal  can  be  felt  is  assurance  of 
safety  against  perforation  which  may  occur  in  any  case. 

There  can  be  no  assurance  of  safety  until  the  apical  tissue  can  be 
explored,  but  perforation  must  be  avoided.  The  fine  Downie  broach 
is  useful  in  difficult  cases,  and,  if  necessary,  a  No.  1  Beutelrock  drill 
may  be  used.  When  the  apical  foramen  is  open,  or  further  work  is 
impossible  without  the  danger  of  perforation,  the  canal  treatment  is 
conducted  upon  the  lines  laid  down  for  gangrenous  pulp.  (See  p. 
579.)  A  difficult  class  of  cases  sometimes  presents  in  which  the 
disease  supervenes  and  where  work  which  may  be  regarded  as  des- 
perate has  been  done,  or  where  pins  have  been  inserted  and  .are 
almost  impossible  of  removal,  as,  for  example,  where  a  Logan  crown, 
has  been  cemented  to  place.  In  such  cases  the  idea  of  Watkins  in 
applying  blue  light  directly  by  means  of  a  funnel  may  be  of  great 
value  in  reducing  inflammation,  and  mild  applications  of  the  x-rays 
or  the  high-frequency  violet  ray  may  be  useful,  but  sometimes  the 
work  must  be  carefully  dismantled  to  permit  retr'eatment.  An  .T-ray 
should  always  be  first  made  as  a  guide. 

If  the  pericementitis  have  been  of  long  standing,  the  thickening 
of  the  membrane  will  have  caused  protrusion  of  the  tooth.  The 
tooth  should  be  ground  off  at  its  point  of  occlusion  until  it  occludes 
with  somewhat  less  force  than  its  neighbors,  the  therapeutic  principle 
in  these  cases  being  that  of  removing  the  source  of  irritation  and 
procuring  surgical  rest.  Indications  of  favorable  results  are  found 
in  the  red  gum  line  assuming  its  normal  position,  tenderness  disap- 
pearing, and  increased  tightness  of  the  tooth. 

This  afi^ection  is  extremely  common  about  the  roots  of  pulpless 
teeth,  and  always  signifies  more  or  less  enforced  disuse  of  the  teeth, 
and,  if  uncorrected,  their  ultimate  loss. 

This  condition  is  sometimes  associated  with  a  chronic  blind  abscess. 
(See  p.  631.)  Upon  treatment,  acute  apical  abscess  is  apt  to  be 
lighted  up;  therefore  the  sterilization  should  be  prolonged  and 
thorough  to  avoid  acute  apical  abscess.  In  one  case  of  a  cyst  asso- 
ciated with  a  lower  molar  tooth  which  had  a  leaky  gutta-percha 
crown  and  partial  canal  filling,  extraction  was  advised  for  reasons 
other  than  canal  treatment.  The  cyst  then  promptly  developed  as 
an  acute  abscess,  which  shifted  its  position  toward  the  cheek  and 
there  discharged  without  production  of  scar. 


SEPTIC  PERICEMENTITIS  AT  BIFURCATIONS  643 

Septic  Pericementitis  at  Bifurcations  of  Multi-rooted  Teeth. — 
Teeth  weakened  by  caries' may  fracture  after  filhng  in  such  a  manner 
that  the  hne  of  fracture  exposes  the  pericementum  at  the  bifurcation. 
The  crack  admits  septic  sahva,  and  a  filhng  or  fiUings  usually  sink 
gingivally,  wedging  apart  the  two  sections  and  admitting  more  or 
less  food  matter.  If  the  canals  of  the  sections  have  been  previously 
treated  and  filled,  it  is  usual  to  find  a  more  or  less  general  peri- 
cementitis due  to  the  wedging  and  septic  irritation.  It  subsides  upon 
sterilizing  by  means  of  a  douche,  while  gentle  broaching  removes  the 
accumulated  debris.  Formocresol,  diluted  with  phenol  camphor  to 
a  5  or  10  per  cent,  formalin  strength,  is  to  be  placed  in  the  pulp 
cavity  and  covered  with  sandarached  cotton,  and  a  ligature  of  silk 
or  wire  is  to  be  tied  about  the  tooth  to  draw  the  parts  together.  A 
hollow  metal  crown  is  to  be  constructed  and  before  placement  a 
little  oxyphosphate  of  copper  or  oxychlorid  of  zinc  cement  is  to 
be  worked  into  the  joint,  which  is  temporarily  sprung  open.  The 
part  may  be  joined  by  amalgam  built  into  a  dove-tail  (Fig.  312), 
or  a  trephine  may  be  driven  into  the  face  of  the  crown  and  a  metal 
ring  be  cemented  into  it  (Fig.  316). 

If  the  canals  be  septic,  an  apical  abscess  may  complicate  the 
condition  and  require  treatment  while  the  fracture  is  being  handled. 
In  some  cases  a  metal  staple  may  be  placed  in  the  canals  of  the  tw^o 
sections  and  so  arranged  as  to  spring  the  parts  together  when  forced 
to  place.  The  joint  should  have  one  of  the  cements  worked  into  it 
before  this  staple  is  cemented  to  place.  About  the  staple  quick- 
setting  amalgam  should  be  packed,  a  copper  band  having  been  pre- 
viously adjusted  to  act  as  a  matrix.  Later,  this  band  is  to  be  removed 
and  a  porcelain-faced  gold  crown  or  a  porcelain  crown  baked  on  a 
heavy  wide  platinum  band  and  cap  arranged  to  sustain  it  (Fig.  294). 

The  staple  may  be  utilized  as  a  portion  of  a  crown  base  of  the 
Richmond  or  other  variety,  the  bifurcation  and  crown  cementing 
being  deferred  until  the  final  operation.  Irritation  may  arise  in 
some  of  these  cases,  which,  however,  need  not  prevent  the  trial  of 
the  method  as  a  last  resort. 

The  methods  of  tooth  salvation  here  indicated  are  subject  always 
to  the  general  principle  of  extraction  when  advisable.  In  no  case 
should  teeth  in  inoperable  condition  be  saved  at  the  expense  of  the 
individual  through  constant  pus  formation. 


CHAPTER  XXI. 
NON-SEPTIC  PERICEMENTITIS. 

Vaeious  grades  of  pericemental  irritation,  ranging  from  a  mild 
arterial  hyperemia  to  actual  inflammation,  may  be  produced  by 
non-septic  causes. 

The  most  satisfactory  evidence  that  inflammation  may  be  so 
caused  is  furnished  by  Talbot's  experiments  with  the  mercurialization 
of  dogs.  Beginning  with  healthy  pericementi,  these  were,  after 
mercuiialization  of  the  animal,  found  to  contain  the  round-celled 
infiltration  characteristic  of  inflammation,  and  no  bacteria  could  be 
found.  Further  evidence  is  given  by  the  usual  experimental  study 
of  inflammation  with  the  mesentery  of  the  frog.  Simple  irritation, 
even  with  antiseptic  substances,  produces  the  phenomena.  Any  of 
the  causes  which  may  produce  inflammation  may,  if  acting  in  more 
mild  degree,  produce  arterial  hyperemia.  If  the  action  of  the  cause 
be  violent  and  then  discontinued,  as  in  the  case  of  a  blow,  the  inflam- 
mation resulting  is  acute,  but  may  pass  into  a  chronic  form;  but  if 
the  cause  continue  to  act  it  produces  a  chronic  inflammation. 

For  purposes  of  description,  non-septic  pericementitis  may  be 
divided,  according  to  its  character,  into  traumatic  and  symptomatic, 
and,  according  to  its  location,  into  apical  and  general. 


TRAUMATIC  PERICEMENTITIS. 

By  traumatic  pericementitis  is  meant  a  profound  irritation  of  the 
pericementum,  the  result  of  mechanical  violence  applied  externally 
to  the  tooth,  or  of  instrumentation  or  chemical  irritation  of  the 
pericementum  through  the  root  canal. 

Causes. — ^Violence  Externally  Applied. — Excessive  force  deliv- 
ered directly  upon  the  teeth,  as  in  case  of  blows,  fafls,  overmafleting 
in  building  fillings,  the  biting  of  nuts,  thread,  or  other  hard  objects, 
or  force  indirectly  delivered,  as  in  case  of  blows  received  under  the 
chin,  bringing  the  teeth  forcibly  together,  may  all  cause  acute  peri- 
cementitis. 

An  excessive  amount  of  filling  on  the  occlusal  surface  of  a  tooth, 
a  maloccluding  crown  or  overful  fillings  upon  the  proximal  aspect, 
(644) 


TRAUMATIC  PERICEMENTITIS  645 

maintaining  a  wedged  condition,  cause  overocclusion  upon  the  tooth 
and  an  irritation  of  its  pericementum. 

The  overstraining  of  the  pericementum  of  a  tooth  as  the  result  of 
overuse,  as  in  cases  where  only  a  few  teeth  remain  for  mastication,  or 
where  pyorrhea  or  calculus  has  caused  resorption  of  the  alveolar 
process  and  looseness  of  the  teeth,  or  where  artificial  dentures  are 
clasped  to  remaining  teeth,  or  where  bridges  are  supported  upon 
insufficient  piers,  are  frequent  causes  of  non-septic  pericementitis  of 
a  degenerative  character.  The  presence  of  a  rough  flaring  or  a  too 
deeply  placed  crown  band  beneath  the  gum  margins,  portions  of 
cement  used  in  cementation  of  crowns,  or  excess  of  filling  material 
beneath  the  gum,  are  all  causes  of  marginal  gingivitis,  with  which 
pericementitis  may  be  associated.  With  these  marginal  cases  septic 
causes  usually  have  to  be  considered  as  complications. 

Too  violent  wedging  is  always  followed  by  more  or  less  peri- 
cementitis of  the  wedged  teeth,  and  their  neighbors,  more  marked 
when  elastic-rubber  wedges  are  used. 

In  correcting  irregularities  of  the  teeth,  if  they  be  moved  too 
rapidly,  are  not  firmly  directed  during  the  operation,  or,  subse- 
quently, not  firmly  maintained  in  position,  pericementitis  of  a  high 
grade  is  frequently  excited.    (See  Overuse  and  Malocclusion  of  Teeth.) 

Violence  Internally  Applied. — If  a  wholly  or  partially  vital 
pulp  be  torn  from  its  apical  connections,  as  in  the  use  of  pressure 
anesthesia,  an  apical  traumatic  pericementitis  may  be  set  up.  This 
is  usually  transient.  Secondary  hemorrhage  may  occur  and  produce 
pericementitis. 

Excessive  laceration  of  the  apical  tissue  by  means  of  barbed 
instruments,  the  inclusion  of  air  or  medicament  under  a  root  dress- 
ing or  filling,  the  same  exercising  pressure  upon  the  apical  tissues; 
the  mechanical  irritation  of  a  projecting  root  filling,  pivot  wire, 
broach,  or  drill,  are  all  sufficient  causes. 

The  undue  enlargement  of  the  apex  of  the  root  canal  or  the  passage 
of  a  reamer  through  the  lateral  aspect  of  a  root  may  excite  inflam- 
mation, and  the  perfect  filling  of  the  opening  may  be  exceedingly 
difficult,  so  that  if  the  tissues  are  not  infected  at  the  time,  sepsis 
may  later  follow. 

Chemical  Irritation. — The  application  of  arsenic  to  a  perfora- 
tion may  excite  inflammation  and  necrosis,  which  endangers  the 
jaw.  (See  p.  528.)  The  use  of  arsenic  as  a  pulp  devitalizer  may 
cause  a  hyperemia  of  the  apical  tissue,  following  the  hyperemia  of 
the  pulp,  and  causing  slight  tooth  extrusion,  which  is  aggravated 
by  the  malocclusion.     This  is  not  dangerous.     (See  p.  521.) 

The  undue  use  of  escharotics,  such  as  carbolic  acid,  sodium  dioxid. 


646  NON-SEPTIC  PERICEMENTITIS 

zinc  chlorid,  sulphuric  acid,  or  mercuric  chlorid,  in  a  pulp  canal 
may  excite  an  undesirable  irritation.  The  limited  irritation  follow- 
ing their  limited  use  is  often  more  than  offset  by  the  advantages  of 
the  asepsis  produced. 

Prophylaxis. — Many  of  these  causes  are  avoidable,  and  operators 
mindful  of  possible  irritations  should  avoid  the  mechanical  irritation 
of  apical  tissues,  neutralize  powerful  acids  or  alkalies,  use  escharotics 
with  caution,  wedge  teeth  gradually,  and  after  wedging  either  pack 
gutta-percha  between  the  teeth  to  permit  them  to  rest  for  a  few 
days  or  fix  them  immovably  with  wooden  wedges  or  steel  separators 
during  malleting. 

During  orthodontia  teeth  should  be  moved  steadily,  and  after 
alignment  is  secured  they  should  be  firmly  maintained  in  position 
until  deposition  of  bone  occurs. 

Patients  should  be  warned  against  the  evil  effects  of  thread  biting 
and  biting  hard  substances. 

Pathology  and  Morbid  Anatomy. — Chemical  substances  applied  in 
excess  cause  a  destruction  of  tissue  dependent  upon  the  quantity 
used.  Inflammation  tending  to  the  resorption  of  the  dead  tissue 
occurs.  The  pericementitis  presumably  persists  in  some  degree 
until  the  foreign  (dead)  material  is  removed  by  natural  processes. 

In  the  case  of  protruding  foreign  bodies,  such  as  root  fillings, 
broaches,  etc.,  there  is  a  tendency  of  the  inflammation  to  become 
subacute  or  chronic.  The  foreign  body  may  to  an  extent  become 
encysted,  particularly  in  the  case  of  a  gutta-percha  root  filling.  In 
other  cases  the  continued  vascular  disturbance,  if  of  mild  degree, 
produces  hypercementosis;  in  more  severe  cases  resorption  of  the 
root  occurs. 

Cases  due  to  perforation  of  the  root  and  wounding  of  the  peri- 
cementum, after  the  acute  symptoms  have  passed,  commonly  assume 
an  irritative  and  chronic  type,  the  soft  tissues  included  in  the  per- 
foration being  in  a  state  of  chronic  inflammation.  Many  of  these 
cases  become  infected  owing  to  the  difficulty  of  completely  sterilizing 
the  apical  portion  of  the  canal  which  lies  beyond  them. 

The  pericementitis  produced  by  pressure  of  included  air,  liquid, 
or  plastic  root  filling  upon  the  apical  tissue  is  often  severe.  Upon 
removal  of  the  root  dressing  or  filling  the  engorgement  is  relieved 
by  the  gushing  of  blood  through  the  root  canal.  The  inflammation 
may,  however,  continue  unless  sedatives  be  applied  to  the  apical 
tissue  via  the  canal. 

In  cases  due  to  traumatism,  such  as  violent  wedging,  rapid  move- 
ment in  regulating,  overmalleting,  blows,  biting  of  thread,  ice,  nuts, 
etc.,  the  condition  is  surgically  one  of  bruise. 


TRAUMATIC  PERICEMENTITIS  647 

The  phenomena  of  active  inflammation  make  their  appearance  to 
an  extent  governed  by  the  degree  of  violence — exudation,  swelling, 
redness,  and  pain;  fibrinous  and  corpuscular  exudations  occur,  and 
later  a  reorganization  of  tissue  occurs,  in  some  cases  a  degeneration, 
depending  upon  the  completeness  with  which  the  indicated  thera- 
peusis  is  applied  and  upon  the  vitality  of  the  pateint. 

Traumatic  pericementitis  in  high  degree  in  the  young  may  be 
recovered  from ;  but  in  the  middle  aged  and  aged  it  may  give  rise  to 
a  series  of  degenerative  changes  which  end  only  with  the  loss  of  the 
tooth. 

In  cases  due  to  looseness  of  the  teeth,  of  course,  septic  primary 
causes  have  to  be  considered,  but  the  pericementitis  may  be  ciuite 
as  much  mechanically  as  septically  produced. 

In  all  cases  the  extrusion  caused  by  the  inflammation  adds  another 
exciting  cause  of  apical  pericementitis — i.  e.,  malocclusion,  which 
aggravates  the  condition. 

Symptoms  and  Diagnosis. — The  amount  of  pericemental  inflamma- 
tion present  is  evidenced  by  the  soreness  and  extrusion  of  the  tooth 
and  the  degree  of  redness  in  the  overlying  gum  tissue. 

A  history  of  violence  may  be  obtained  when  it  has  occurred.  Mal- 
occlusion may  be  detected  by  occlusion  marks  upon  fillings  or  by 
means  of  carbon  paper.  The  untoward  results  of  canal  operations 
may  be  inferred  from  a  personal  knowledge  of  the  case  or,  perhaps, 
from  the  history.  It  is  at  times  difficult  to  exclude  septic,  non- 
purulent, apical  pericementitis  as  a  cause,  particularly  if  the  case 
come  from  the  hands  of  another  practitioner.  In  doubtful  cases 
the  treatment  for  inferred  traumatisms  may  be  employed,  and  if 
followed  by  good  results  a  j^ost  hoc  diagnosis  of  traumatic  peri- 
cementitis may  be  made.  The  a'-rays  afford  a  means  of  determining 
extruding  root  fillings,  broaches,  etc. 

Treatment. — Foreign  bodies  protruding  from  the  root  apex  must 
be  removed  if  persistent  symptoms  demand  it.  This  may  require 
an  artificial  opening  for  its  performance,  or  root  amputation.  Per- 
forations should  be  Carefully  treated. 

If  evidence  of  pericementitis  persist,  the  end  of  the  root  including 
the  perforation  should  be  amputated,  or  if  the  tooth  persistently 
extrude,  the  tooth  may  be  extracted,  the  perforation  and  canal  filled 
Math  gold  or  gutta-percha,  and  the  tooth  replanted  under  antiseptic 
precautions. 

In  all  cases  due  to  violence  the  treatment  is  that  adapted  to  injury; 
first,  surgical  rest  of  the  pericementum.  This  may  be  accomplished 
in  two  ways:  either  by  preventing  the  tooth  striking  its  antagonists 
or  holding  it  so  rigidly  that  it  cannot  move  if  it  does  meet  them. 


648  NON-SEPTIC  PERICEMENTITIS 

As  a  preliminary  measure  the  tooth  is  gently  but  firmly  lashed 
to  its  neighbors  by  means  of  ligatures  so  that  it  is  rigidly  held.  A 
swaged  cap  is  either  fitted  to  a  neighboring  tooth,  or  the  antagon- 
izing teeth  are  ground  away  until  they  fail  to  strike  the  injured 
tooth;  the  first  method  is  to  be  preferred. 

In  cases  involving  several  teeth,  such  as  all  of  the  incisors,  two 
metallic  plates  are  quickly  swaged  to  cover  posterior  teeth  and  raise 
the  bite,  and  they  are  cemented  in  position  to  relieve  the  irritated 
teeth  from  occlusion. 

When  the  apical  tissues  have  been  irritated  by  way  of  the  canal, 
sedatives,  such  as  strong  tincture  of  aconite  or  menthol  in  chloroform 
phenol-camphor,  eugenol,  or  menthol-phenoP  (menthol,  3  parts; 
carbolic  acid,  1  part;  melted  together)  or  thymophen  should  be 
applied  on  cotton  to  the  apical  tissue  by  way  of  the  root  canal.  All 
cases  of  traumatic  pericementitis  require  the  persistent  use  of  counter- 
irritants,  applied  every  other  day  to  the  overlying  gum.     (See  p.  476.) 

Systemic  derivation  is  also  useful  in  the  acute  cases.  In  even 
mild  cases  not  due  to  violence  the  guarding  of  the  extruded  tooth 
against  malocclusion  is  of  advantage. 

If  the  cause  be  some  mechanical  irritant  at  the  gum  margin,  this 
should  be  removed  and  the  case  treated  as  above  described.  Recog- 
nizing the  possible  influence  of  septic  causes,  oral  antiseptics  are  to 
be  used. 

SYMPTOMATIC  NON-SEPTIC  PERICEMENTITIS. 

By  symptomatic  non-septic  pericementitis  is  meant  an  aseptic 
pericementitis  occurring  as  the  result  of  systemic  conditions,  or  of 
the  action  of  drugs  taken  internally. 

If  mercury  be  administered  to  patients  in  large  doses  for  long 
periods,  or  in  one  or  more  massive  doses,  or  if  the  patient  have  an 
idiosyncrasy  to  the  action  of  this  agent,  or  be  a  worker  in  mercurials, 
an  irritation  of  the  salivary  glands  is  excited,  followed  by  looseness 
and  soreness  of  the  teeth  and  swelling  of  the  gums;  that  is,  a  general 
pericementitis  and  maxillary  periostitis  arise.  The  patient  has  a 
metallic  coppery  taste,  coated  tongue,  and  fetid  breath;  the  gums 
are  puffy  and  bleed  easily.  In  advanced  cases  the  tongue  and  cheeks 
are  swollen.  Potassium  iodid  administered  in  this  condition  relieves 
the  maxillary  periostitis  and  pericementitis;  but  the  same  drug 
administered  in  health,  or  for  conditions  other  than  mercurial 
poisoning,  also  causes  irritation  of  the  pericementum.     Pilocarpin 

1  Dr.  Morgan  Howe. 


SYMPTOMATIC  NON-SEPTIC  PERICEMENTITIS  649 

has  a  similar  effect,  though  in  much  less  degree.  All  of  these  drugs 
are  partially  eliminated  by  the  glandular  appendages  of  the  mouth, 
and  during  elimination  apparently  act  as  local  irritants.  Lead 
poisoning  may  have  a  similar  action.  A  blue  line  appearing  on  the 
gums  is  symptomatic.  It  occurs  in  painters  and  workers  in  lead. 
Lead  has  been  found  in  the  calculus  on  the  teeth  and  even  in  the 
tooth  substance. 

Patients  who  have  a  gouty  heredity,  or  who  are  the  subjects  of 
active  gout,  frequently  exhibit  a  tenderness  of  the  entire  pericemen- 
tum of  one  or  more  or  sometimes  all  of  the  teeth.  This  pericemental 
disturbance  may  be  the  precursor  of  an  acute  outbreak  of  gout  in 
the  metatarsophalangeal  joint. 

Scurvy — a  very  rare  systemic  disease — is  attended  by  rapid 
degeneration  of  the  pericementum  of  the  teeth  and  of  the  alveolar 
tissues. 

Syphilis  is  also  attended  by  pericemental  irritation.  This,  of 
course,  is  of  septic  origin. 

Talbot's  experiments  on  dogs  show  conclusively  that  a  true  peri- 
cementitis may  be  induced  owing  to  the  chemotactic  properties  of 
the  mercury  alone.     (See  Interstitial  Gingivitis.) 

In  auto-intoxication  by  intestinal  toxins  or  by  leukomains  in 
diseases  involving  general  malnutrition,  the  irritants  are  probably 
in  part  eliminated  by  the  gums,  which  are  in  turn  irritated.  (See 
Pyorrhoea  Alveolaris.) 

It  has  been  shown  by  Loup  that  mercurial  stomatitis  may  be 
cured  by  mercury  used  as  an  oral  antiseptic;  therefore,  the  logical 
conclusion  is  that  oral  organisms  play  a  part  in  the  production  of 
the  local  effects  of  mercury;  probably  the  mercury  produces  a  local 
predisposition.  This  is  further  confirmed  by  the  fact  that  if  the 
teeth  are  attended  to  and  oral  prophylaxis  be  practised  before  the 
administration  of  mercury  to  syphilitics,  they  tolerate  greater 
amounts  of  the  drug  before  salivation  or  stomatitis. 

Treatment. — The  drug  should  be  discontinued,  the  disease,  if 
present,  should  be  antagonized,  and  the  local  complications,  if  any, 
should  be  appropriately  treated,  antisepsis  being  always  advisable. 
If  the  pericementitis,  gingivitis,  and,  stomatitis  be  mercurial,  the 
drug  should  be  stopped  and  an  antisialagogue  used,  such  as  atropin 
sulphate,  ^^  gr.  each  four  to  six  hours,  until  relieved. 

Potassium  chlorate  as  a  mouth  wash,  or  internally,  is  useful  if  the 
stomach  is  not  irritable. 

I^ — Potassii  chloratis gr.  xlviij 

Tr.  myrrhse .     f  3  ss 

Elixir  calisayae q.  s.  adfgiij — M. 

Sig. — Teaspoonful  every  five  hours,  or  use  as  a  mouth  wash.     (Hare.) 


650  NON-SEPTIC  PERICEMENTITIS 

Results  of  Chronic  Non-septic  Pericementitis. — If  at  any  point  of 
the  irritated  pericementum  a  constructive  grade  of  irritation  be 
maintained,  the  cemental  tissue  becomes  hypertrophied  (Fig.  590). 
If  a  more  severe  grade  of  irritation — i.  e.,  low-grade  inflammation 
— be  present  for  a  long  time,  the  cementum  and  even  the  dentin 
of  the  root  may  be  resorbed.  Both  of  these  results  may  go  on 
concurrently  at  different  points,  or  resorption  may  be  followed  by 
deposition  of  cementum  if  the  conditions  change. 

Chronic  overuse  or  disuse  of  teeth  results  in  degenerations  of  the 
pericementum.     (See  p.  661.) 

HYPERCEMENTOSIS  (DENTAL  EXOSTOSIS,  EXCEMENTOSIS, 
HYPERPLASIA  OF  THE  CEMENTUM). 

Definition. — By  hj^percementosis  is  meant  a  secondary  deposit,  or 
an  increase  of  volume  of  the  cementum  of  a  tooth  beyond  the  normal 
limit.     It  may  be  circumscribed  or  diffuse. 

Causes. — A  constructive  degree  of  hyperemia  or  very  mild  inflam- 
mation is  the  proximate  cause,  which  may  be  excited  by  numerous 
primary  causes,  such  as  a  projecting  root  filling,  a  projecting  edge  of 
crown  filling,  deposist  of  salivary  calculus,  the  overlapping  of  a  cavity 
margin  by  the  gum,  malocclusion,  non-occlusion,  the  biting  of  hard 
objects,  such  as  nuts  or  thread,  the  overuse  of  certain  teeth,  the 
habitual  tapping  together  of  teeth,  the  habitual  chewing  of  tooth- 
picks, the  gradual  pressure  of  gas  from  dead  pulps.     The  pressure  of  a 

Fig.  590 


tooth  root  against  another  root  during  eruption  is  a  sufficient  cause. 
(See  Fig.  173.)  The  overcrowding  of  teeth  in  an  arch  has  also 
caused  this  condition,  as  has  also  the  impaction  of  a  tooth  (Fig.  218). 
Chronic  alveolar  abscess  or  pyorrhea  alveolaris  may  cause  it  by 
inducing  about  itself  at  a  distance  an  area  of  hyperemia.  (Aseptic 
Area.)  It  also  seems  at  times  to  be  induced  after  pulp  devitalization 
from  any  cause.  Hypercementosis  is  a  possibility  in  any  case  of 
chronic  pericemental  irritation;  it  represents  a  degree  of  irritation 


HYPERCEMENTOSIS 


651 


rather  than  any  one  specific  cause.  It  has  been  discussed  by  some 
writers  under  the  heading  of  Constructive  or  Condensing  Perice- 
mentitis,  and  is  fairly  analogous  to  osteosclerosis.     (See  p.   144.) 


Fig.  591 


'  Hypercementosis.      (Skiagraph  by  Lodge.) 

Situation. — Hypercementosis  may  be  diffused  over  almost  an 
entire  root  or  several  roots,  or  be  localized  as  a  distinct  nodule  at 
some  lateral  aspect,  or  exist  as  a  circumscribed  enlargement  about 
the  apex  of  a  root,  or  at  the  neck  of  a  root.  It  is  always  located 
where  the  cause  (hyperemia)  has  been  produced  (Fig.  590). 


Fig.  592 


:'\^'r^ 


Hypertrophy  of  the  cementum  on  the  side  of  a  root  of  a  lower  molar  near  the  neck 
of  the  tooth  of  a  man:  o,  dentin;  6,  cementum;  c,  fibers  of  peridental  membrane; 
from  6  to  c  the  cementum  is  normal  and  the  incremental  lines  fairly  regular,  but  at 
d  one  of  the  lamellse  is  greatly  thickened;  at  e  this  lamella  is  seen  to  be  about  equal 
in  thickness  with  the  others.  The  next  two  lamellse  are  thin  over  the  greatest  prom- 
inence, but  one  is  much  thickened  at  gr,  and  both  at  h.  These  latter  seem  to  partiallj^ 
fill  the  valleys  which  were  occasioned  by  the  first  irregular  growth.  From  a  length- 
wise section.     (Black.) 


Flagg  noted  that  75  per  cent,  of  cases  of  hypercementosis  were 
found  upon  posterior  teeth,  and  that  the  teeth  were  usually  of  the 
character  termed  dense — /.  e.,  the  tissues  of  the  individual  were  of 
recuperative  type,  tending  to  produce  constructive  changes. 


652 


NON-SEPTIC  PERICEMENTITIS 


Pathology  and  Morbid  Anatomy. — For  some  time  after  eruption 
the  cementum  consists  of  but  few  lamellae  of  deposit.  It,  however, 
reaches  a  maximum  normal  development  at  which  it  normally  rests, 
as  in  the  case  of  the  physiological  pulp  cavity.  As  age  progresses 
it  is  apt  to  be  more  thickly  deposited  at  the  expense  of  the  peri- 
cementum, which  becomes  more  attenuated.  Whether  this  is  due  to 
irritants  floating  in  the  blood  stream,  or  to  the  various  local  irritants 
above  mentioned,  or  to  perfectly  normal  development,  is  not  clear 
except  for  certain  definite  cases. 

Nodular  and  irregular  forms  arising  from  the  general  surface  are 
clearly  of  abnormal  type. 

Fig   593 


Apex  of  root  of  an  upper  bicuspid  tooth  with  irregularly  developed  cementum: 
a,  a,  dentin;  b,  b,  pulp  canals.  The  lamellae  of  cementum  are  marked  1,  2,  3,  etc; 
d,  d,  d,  absorption  areas  that  have  been  refilled  with  cementum.  It  will  be  seen  that 
the  apices  of  the  roots  were  originally  separate,  but  became  fused  with  the  deposit 
of  the  second  lamella  of  cementum,  and  that  in  this  regular  growth  began  and  was 
most  pronounced.  It  has  continued  through  the  subsequent  lamellis  but  in  less  degree. 
It  will  also  be  noticed  that  the  absorption  areas,  d,  d,  d,  have  proceeded  from  certain 
lamelliB.  That  between  the  roots  has  broken  through  the  first  lamella  and  pene- 
trated the  dentin,  and  has  been  filled  with  the  deposit  of  a  second  lamella.  Other 
of  the  absorptions  have  proceeded  from  lamellae  which  can  be  readily  made  out.  The 
small  points,  e,  seem  to  have  been  filled  with  the  deposit  of  the  last  layer  of  cementum, 
while  others  have  one,  two,  or  more  layers  covering  them.     (Black.) 


Successive  lamellae  are  deposited;  the  pericementum  recedes, 
causing  resoprtion  of  the  alveolar  process.  Union  of  the  bone  and 
cementum  (ankylosis)  very  rarely  occurs.  A  resorption  of  cementum 
and  dentin  may  occur  at  some  point  owing  to  a  different  degree  of 


HYPERCEMENTOSIS  653 

irritation,  and  in  the  area  a  new  deposition  of  cementum  may  occur 
(Fig,  593,  d).  In  some  cases  distinct  areas  of  hypercementosis  and 
root  resorption  are  seen  in  close  proximity.  Chronic  apical  abscess 
may  produce  a  denudation  of  the  root  end,  and  a  short  distance 
below  an  annular  ridge  of  hypercementosis  may  occur.  Areas  of 
hypercementosis  may  be  translucent  or  decidedly  opaque,  and 
sometimes  the  two  are  combined,  a  mottled  appearance  being  pro- 
duced. 

If  the  growth  proximate  another  root,  the  pericementum  may 
resorb  at  the  point  of  contact  and  a  deposition  of  cementum  occur 
which  firmly  unites  the  roots  in  a  union  called  concrescence.  (See 
p.  263.) 

It  has  occurred  that  a  root  filling  protruding  through  a  perforation 
has  caused  a  diffused  exostosis  of  the  alveolar  process.^  The  hyper- 
trophied  process  may  be  ivory-like  in  hardness. 

Symptoms  and  Diagnosis. — Many  cases  exist  without  active  local 
symptoms.  In  no  case  is  the  color  of  the  gum  altered  unless  other 
disease  than  hyperemia  be  acting  as  a  cause.  In  some  cases  there 
are  symptoms  of  hyperemia  expressed  as  a  disposition  to  bite  hard 
upon  the  particular  tooth,  or  to  grind  upon  it.  A  paroxysm  of  gnaw- 
ing pain  lasting  for  some  hours,  and  recurring  at  intervals,  is  also 
somewhat  characteristic.  Sympathetic  hyperemia  of  the  pulp  with 
increased  response  to  thermal  changes  may  occur.  (See  p.  469.) 
The  gum  may  have  slightly  receded. 

Neuralgia,  functional  bhndness,  functional  deafness,  chorea, 
epileptiform  fits,  paralysis,  cardiac  neuralgia,  insanity,  and  other 
related  conditions  have  been  cured  by  the  extraction  of  hyper- 
cementosed  teeth.^ 

The  treatment  of  teeth  presenting  obstinate  symptoms  of  peri- 
cementitis, apparently  due  to  moist  gangrene  of  the  pulp,  may  at 
times  be  complicated  by  unsuspected  hypercementosis. 

In  such  cases,  if  pulp  or  pericemental  complication  cannot  be 
determined,  suspicion  should  point  to  hypercementosis  and  an  .T-ray 
examination  be  made,  by  which  means  the  condition  may  be  posi- 
tively determined.  As  entire  dentures  have  been  extracted,  tooth 
by  tooth,  in  a  vain  endeavor  to  cure  a  neuralgia  about  the  head, 
this  means  of  diagnosis  should  not  be  overlooked. 

Treatment. — The  treatment  for  hypercementosis  may  first  be  a 
conservative  one  if  only  slight  annoyance  be  produced  by  it. 

Counterirritation — correction  of  malocclusion,  etc. — may  be  em- 
ployed.   The  symptoms  may  disappear.     If  they  do  not,  or  they 

1  Garretson's  Oral  Clinic,  1884. 

2  Brubaker.     American  System  of  Dentistry. 


654  NON-SEPTlC  PERICEMENTITIS 

are  severe  when  the  patient  appHes,  the  tooth  should  be  completely 
extracted.  The  operation  of  amputation  of  the  root  end  might  be 
safely  tried  for  apical  hypercementosis,  but  there  are  no  records  of  its 
employment  as  a  means  of  cure.  The  bulbous  condition  of  the  root 
end  may  cause  extraction  to  be  difficult,  and  fracture  of  the  root  end 
may  occur.  Flagg  recommended  that  in  such  a  case  a  fissure  drill 
be  passed  about  the  circumference  of  the  root  end  to  remove  the  bony 
obstruction  to  its  passage  out  of  the  alveolus,  after  which  it  may 
be  lifted  away  with  tweezers.  In  another  method  the  root  may  be 
perforated  by  a  drill  and  then  divided  into  two  sections  by  means  of 
a  dentate  fissure  bur,  after  which  the  halves  may  be  pushed  together 
with  a  small  elevator.  If  not  then  removable  the  fissure  bur  can 
now  easily  enlarge  the  alveolar  constriction.  Cocain  may  be  used 
as  an  obtundent.  The  use  of  alveolar  forceps  for  the  condition  is 
little  short  of  brutal,  and  only  warranted  by  the  impracticability 
of  other  means. 

Extraction  for  hypercementosis  may  cause  considerable  bruising 
of  the  walls  of  the  alveolus,  followed  by  excruciating  pain  lasting 
often  for  days.  The  alveolus  may  refuse  to  granulate,  and  a  septic 
condition  result.  The  pain  has  at  times  been  relieved  by  the  injec- 
tion of  a  2  per  cent,  solution  of  cocain  or  novocain  into  the  gum 
on  either  side  of  the  alveolus,  after  which  the  surfaces  of  the  alveolar 
walls  should  be  sterilized  and  burred  away  until  tissue  capable  of 
granulation  is  reached. 

The  alveolus  should  then  be  irrigated  and  a  clot  invited  by  causing 
a  slight  hemorrhage.     (See  p.  634.) 

ANKYLOSIS  (SYNOSTOSIS). 

By  this  is  meant  the  union  of  bone  and  cementum,  a  condition 
analogous  to  ankylosis  of  bone. 

Hopewell-Smith^  has  described  5  cases,  of  which  he  offers  the 
following  explanation:  (1)  inflammation  occurs  and  the  membrane 
is  changed  into  granulation  tissue;  (2)  the  cellular  elements  destroy 
portions  of  the  bone  and  excavate  the  cementum;  (3)  the  mass  of 
granulation  tissue  is  then  ossified,  joining  the  bone  and  cementum 
in  a  firm  union. 

E.  C.  Rice^  has  reported  a  case  of  a  lady  for  whom  an  implantation 
of  an  upper  bicuspid  was  done.  In  an  effort  made  later  to  remove 
the  tooth  all  attempts  to  loosen  it  in  any  degree  with  forceps  failed. 

In  my  own  practice  an  implanted  tooth  is  firmly  immovable  in 

1  Histology  and  Pathohistology  of  the  Teeth. 

2  Private  communication. 


RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH     655 

any  degree,  though  several  years  in  place.  The  union  may  not  be 
a  true  ankylosis  in  these  cases,  though  doubtless  bone  has  entered 
areas  of  previous  resorption.  A  remarkable  case  was  shown  the 
editor  by  Dr.  J.  Curry,  of  Philadelphia.  Every  pier  tooth  of 
four  bridges  was  firmly  ankylosed  and  immovable,  yet  large  bays 
of  resorption  in  each  root  necessitated  extraction.  This  was  not  a 
plantation  case. 

Fig.  594 


Vertical  section  of  a  human  tooth  ankylosed  to  the  jaw:  R,  root;  B,  bone  of  jaw. 
The  absolute  continuity  of  the  two  hard  tissues  is  strikingly  shown.  From  the  col- 
lection of  the  late  Storer  Bennett. ^    (Hopewell-Smith.) 


RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH. 

By  resorption  of  the  roots  of  permanent  teeth  is  meant  the  gradual 
removal  of  the  cementum  and  dentin  of  permanent  roots  by  phago- 
cytic cells  existing  in  the  adjacent  soft  tissue  (osteoclasts).  When 
occurring  as  the  result  of  pressure  by  another  tooth  a  tissue  similar 
to  an  absorbent  organ  (See  p.  218),  as  in  resorption  of  deciduous 
teeth,  is  probably  developed  between  them. 

Causes. — The  proximate  cause  is  probably  in  all  cases  a  degree  of 
irritation  greater  than  that  required  to  produce  hypercementosis. 
Probably  a  mild  non-septic  inflammation  exists.  Talbot's  demon- 
strations of  interstitial  gingivitis,  a  term  meant  to  include  interstitial 

1  Transactions  of  the  Odontological  Society  of  Great  Britain. 


656 


NON-SEPTIC  PERICEMENTITIS 


pericementitis,  show  that  it  is  a  frequent  cause  of  both  root  and 
alveolar  resorption.  (See  Deeply-seated  Gingivitis.)  In  other 
words,  it  is  due  mainly  to  an  aseptic  pericementitis. 

The  disease  has  been  discussed  by  other  writers  as  "Rarefying 
Pericementitis,"  fairly  analogous  to  osteoporosis.     (See  p.  144.) 


Fig.  595 


Fig.  596 


Fig.  597 


Fig.  595. — Apical  abscess  and  resorption,  produced  by  a  protruding  broach. 

Fig.  596. — -Deciduous  cuspid  crowned,  mistaken  for  .permanent  cuspid  which  lay 
in  jaw  and  caused  resorption  of  root  of  permanent  lateral.     (Skiagraph  by  Price.) 

Fig.  597. — Resorption  at  cervical  third  in  two  replanted  teeth,  one  broken  in 
consequence.     Editor's  practice.     (Skiagraph  by  Hagopian.) 


Fig.  598 


Fig.  599 


Case  of  extensive  resorption  about  upper 
central.     (Skiagraph  by  Lodge.) 


Resorption  of  roots.      (Skiagraph 
by  Lodge.) 


Of  primary  causes  chronic  apical  abscess  seems  to  be  a  frequent 
one.  Although  theoretically  the  alkaline  pus  formed  should  neutral- 
ize acid  formation,  the  fact  of  resorption  remains,  and  is  probably 
explainable  upon  the  ground  that  it  is  produced  by  the  granulation 
tissue  formed  about  the  root  apex  during  periods  of  lessened  pus 
formation. 

Protruding  root  fillings  or  broaches  are  common  causes  (Fig.  595). 
Plantations  are  frequently  followed  by  it.     A  peculiar  resorption 


RESORPTION  OF  THE  ROOTS  OF  PERMANENT  TEETH     657 

in  the  cervical  third  of  two  replanted  incisors  caused  the  fracture 
of  one  at  the  point  of  resorption  and  necessitated  the  removal  of 
both  teeth  (Fig.  597).  Plantations  are  usually  followed  by  peculiar 
resorptions  over  even  the  entire  root.  Looseness  of  a  tooth  with  the 
resultant  excess  of  movement  excites  deeply-seated  gingivitis  and 
resorption  of  bone  and  often  of  roots.  Partial  luxation  as  the  result 
of  a  blow  or  fall  produces  the  same  result,  the  pericementum  becom- 
ing thickened,  the  tooth  loosened  and  extruded,  and  malocclusion, 
which  is  also  a  cause,  being  induced. 

A  toothpick  broken  off  in  the  gum  tissue  has  produced  resorption 
at  the  neck  of  the  root. 

Fig.  600 


Inflamed  pericementum,  osteoclasts  in  Howship's  lacunse.     (V.  A.  Latham  ) 


The  descent  of  a  supernumerary  or  impacted  tooth  upon  a  per- 
manent root  has  caused  resorption,  exposing  the  pulp  of  the  resorbed 
root,  and  producing  pulp  reactions.  This  may  be  quite  extensive 
before  violent  symptoms  occur  (Fig.  596).  In  one  case  both  the 
buccal  roots  of  an  upper  molar  were  removed  by  a  supernumerary 
tooth,  the  crown  of  which  fitted  the  resorbed  root  ends. 

Resorptions  also  occur  in  orthodontia,  as  when  a  cuspid  is  delayed 

and  presses  upon  a  lateral  root.   The  resorption  may  be  more  distant 

than  the  pressure  point.     In  orthodontia  this  may  be  explained 

by  the  extension  of  the  phagocytic  area  or  the  induction  of  such  an 

42 


658  NON-SEPTIC  PERICEMENTITIS 

area  about  moving  teeth;  indeed,  teeth  cannot  be  moved  without 
exciting  a  phagocytic  action. 

Dewey/  following  Hertzler,  claims  that  rickets  causing  imperfect 
calcification  of  teeth  is  liable  to  be  a  factor  in  untoward  resorptions 
in  orthodontia,  while  tuberculosis  neither  interferes  with  tooth, 
eruption  nor  calcification,  but  may  interfere  with  proper  physio- 
logical resorption  because  the  phagocytes  are  elsewhere  occupied  and 
the  absorbent  organ  is  not  fully  developed. 

Calculus  beneath  the  gum  margin  has  produced  resorption  through 
the  production  of  gingivitis.  In  one  case  noted  four  lower  incisors 
presented  the  characteristic  bays  at  a  point  one-eighth  inch  below 
the  gum  line. 

Some  of  the  cases  exhibit  no  tangible  cause;  the  root  resorbs 
apparently  as  the  result  of  a  peculiar  reaction  upon  the  part  of  the 
tissues  of  the  individual,  who  may  lose  many  teeth  by  this  process — 
i.  e.,  a  dyscrasia  exists.  The  teeth  may  be  non-carious  and  the  pulps 
vital.  In  some  of  these  cases  neurasthenia  or  a  uric  acid  diathesis 
seems  to  have  some  association  wdth  the  condition  (Fig.  601). 

Pathology  and  Morbid  Anatomy. — Both  resorption  of  cementum 
and  its  redeposition  occur  in  deciduous  teeth  as  physiological  pro- 
cesses; at  some  aspect  of  the  cementum  the  tissue  becomes  hollowed 
out,  and  later  filled  in  by  new  cementum.  Resorption  of  tissue 
throughout  the  body  is  accomplished  by  means  of  multinucleated 
cells  (giant  cells,  osteoclasts).  At  some  part  to  be  physiologically 
resorbed  these  cells  make  their  appearance  in  contact  with  the 
tissue  to  be  removed,  and  it  gradually  disappears,  the  layer  of  multi- 
nucleated cells  constantly  occupying  the  excavated  territory  known  as 
Howship's  lacunse  (Figs.  73  and  600). 

If  a  foreign  (aseptic)  body  be  introduced  into  living  tissues,  it 
becomes  surrounded  by  these  cells,  which  in  some  cases  effect  its 
removal;  in  others,  failing  to  remove  the  foreign  body,  connective 
tissue  forms  about  it  and  encysts  it;  encystment  may  occur  after 
partial  removal  by  giant  cells. 

The  resorption  of  a  root  may  be  of  any  extent,  from  a  slight  spicular 
roughness  of  the  apex  of  the  root  to  almost  complete  removal  of 
the  root. 

Perforation  of  the  root  from  side  to  side  may  occur,  of  course, 
involving  the  pulp  canal,  and,  if  the  pulp  be  alive,  obscure  reactions 
upon  its  part  may  occur  (Fig.  601). 

An  area  of  marked  resorption  may  occur  at  a  point  just  beneath 
the  gum  margin  and  upon  any  aspect  of  the  tooth.     In  this  situation 

litems  of  Interest,  May,  1914.  p.  358. 


RESORPTION  OF   THE  ROOTS  OF  PERMANENT  TEETH     659 

it  may  simulate  a  cavity  of  decay  beneath  the  gum.  It  occurs 
upon  either  vital  or  devitalized  teeth,  and  may  expose  the  pulp 
of  the  root-canal  filling.  The  gum  tissue  is  usually  found  within 
the  cavity. 

It  is  probable  that  in  plantations  the  root  acts  as  an  aseptic  foreign 
body;  mild  inflammation  occurs,  subsides,  and  giant  multinucleated 
cells  attack  the  tooth  root  and  endeavor  to 
remove  it  by  solution;  this  they  accomplish,  ^^°'-  ^^^ 

in  part,  in  spots;  then  a  tolerance  is  estab- 
lished and  connective  tissue  organizes  about 
the  roots;  later,  more  complete  regeneration  is 
represented  in  the  formation  of  bone;  condition 
of  a  bony  fixation  is  established,  evidenced  by 
the  clear  ringing  note  elicited  upon  tapping  the 
planted  tooth. 

'■  IP  •  !>  1  Idiopathic   resorption 

With  reference  to  resorption   after   planta-  of  permanent  root.  The 

tions,  Milleri  records  the  following  results  of  ^^J^/fj,"^'  ^^^  ^"^^  7/. 

his  observations.     The  fixation  of  reimplanted  f orated    the    root    as 

or  transplanted  teeth  may  be  accomplished  in  shown.    Crater-hke  re- 

•^  1/  X-  sorption     about     apical 

three  ways:  foramen.     Pulp  first  de- 

1.  By  simple  encapsulation  of  the  root.  vitalized  on  account  of 

"  ^         11  I.  •  •  1  •    1         persistent  pam  and  the 

2.  By  the  bundles  of  connective  tissue  which     tooth  later  extracted. 
fill  up  irregular  absorption  spaces,   especially 

where  the  pericementum  has  not  been  present  at  that  portion  when 
the  implantation  was  made  (a  pseudo-attachment). 

3.  By  direct  union  of  the  surrounding  tissues  with  the  living 
pericementum.  He  inchnes  to  think  this  the  only  permanent 
attachment. 

He  states  that  for  the  most  part  osteoclasts  were  few  and  that 
resorption  was  carried  on  by  small  round  cells. 

The  inflammatory  reaction  and  resorption  is  least  when  replanta- 
tion is  practised,  but  may  at  times  be  pronounced  in  even  those 
cases.  If  the  socket  of  a  tooth  extracted  for  resorption  be  examined, 
a  mass  of  soft  tissue  will  be  found  occupying  the  locations  corre- 
sponding to  the  areas  of  resorption  (Fig.  602) .  No  acid  reaction  can 
be  detected  wdth  litmus  paper,  but,  nevertheless,  it  is  probable  that 
the  cells  producing  resorption  excrete  an  acid  capable  of  dissolving 
the  tissue. 

There  is  some  evidence  of  this  in  cases  of  enamel  resorption  occur- 
ring upon  the  crowns  of  impacted  teeth  which  have  never  been  in 
relation  with  the  oral  fluids,  and  about  which  there  is  no  evidence  of 

1  Independent  Practitioner,  1887 


660 


NON-SEPTIC  PERICEMENTITIS 


caries  in  the  areas  of  dentin  resorption  also  present.  In  the  fortunate 
specimens  of  these  cases  a  superficial  decalcification  of  the  enamel 
surface  may  be  seen  which  can  only  occur  as  the  result  of  acid  action. 
(See  p.  312.) 


Fig.  602 


Resorption  of  distal  root  of  a  first 
molar.     (Skiagraph  by  Custer.) 


Diagram  of  a  case  of  root  resorption 
after  secondary  dentin  had  formed:  SD, 
secondary  dentin;  AR,  area  undergoing 
resorption;  peculiar  central  spire  of  sec- 
ondary dentin  which  has  resisted  the 
resorbeht  action.  Specimen  in  possession 
of  Dr.  A.  P.  Fellows. 


Symptoms  and  Diagnosis. — The  tooth  may  present  symptoms 
of  non-septic  pericementitis,  and  may  be  loosened  in  advanced 
cases.  In  the  early  stages  no  looseness  may  be  observed  until  a 
strain  suddenly  applied  causes  a  luxation;  thereafter  the  tooth 
progressively  loosens. 

The  condition  may  be  discovered  by  accident;  evidences  of  mild 
pericementitis  appear,  and  the  pulp  canal  is  opened  to  search  for 
a  cause.  The  pulp  may  be  found  alive;  if  alive,  and  it  is  killed,  or 
if  it  is  found  dead,  broaches  pass  suddenly  into  the  mass  of  soft 
tissue  underlying  the  root.  The  progressive  loosening  of  the  tooth, 
with  its  peculiar  movement,  is  about  the  only  constant  symptom  of 
the    condition. 

In  cases  of  live  pulp  this  organ  may  be  hyperemic,  so  that  increased 
response  to  heat  or  cold  is  felt;  this,  taken  in  connection  with  the 
tenderness  upon  percussion  which  can  usually  be  elicited,  and  with 
the  peculiar  loosening  of  the  tooth,  is  a  diagnostic  guide. 

Flagg^  stated  that  refiex  neuralgias  occur  in  this  condition,  but 
that  the  most  constant  indication  noted  by  him  was  a  sense  of  dis- 
comfort about  the  jaws,  vaguely  associated  with  some  one  tooth. 
The  patient  is  convinced  that  if  the  tooth  were  removed  relief  would 
follow.  In  the  absence  of  the  loosening,  which  may  not  occur  until 
the  root  is  nearly  gone,  the  resorption  is  most  commonly  discovered 
by  entering  the  pulp  canal  and  finding  its  length  much  shortened. 
In  some  cases  the  resorption  may  be  found  near  the  gum  margin  and 
simulating  a  cavity  of  decay,  from  which  it  may  readily  be  diagnos- 


'  Lecture  on  Dental  Therapeutics. 


OVERUSE  OF  TEETH  661 

ticated  by  its  appearance  when  exposed  by  packing  the  gum  away. 
Such  cases  appear  to  accompany  a  marginal  gum  resorption. 

The  x-rays  should  exhibit  the  condition  with  sufficient  clearness 
to  furnish  an  absolute  diagnosis. 

Treatment. — If  a  diagnosis  can  be  made,  the  tooth  should  be 
extracted  except  in  the  cases  near  the  gum  margin  alone,  which  may 
be  filled  with  plastic  fillings.    Even  then  the  condition  may  progress. 

DEGENERATION  OF  THE  PERICEMENTUM. 

Strictly  speaking,  the  overuse,  abuse,  and  disuse  of  the  teeth  are 
causes  which  produce  a  general  hyperemia  or  inflammation  of  the 
pericementum  (non-septic  pericementitis).  If  continued,  the  inflam- 
mation extends  into  the  gum  tissue  and  a  deep-seated  gingivitis  is 
produced.  The  results  of  the  causes  are,  therefore,  classifiable  under 
either  non-septic  pericementitis  or  deeply-seated  gingivitis.  Either 
of  these  conditions  renders  the  tissues  involved  liable  to  the  degen- 
erations and  resorptions  which  accompany  continued  inflammation, 
or  acts  as  a  predisposing  cause  to  local  infection  by  oral  organisms, 
beginning  its  action  at  the  gum  margin,  and  which  sooner  or  later 
produces  a  purulent,  or  apparently  non-purulent,  liquefaction  of  the 
gingival  portion  of  the  pericementum  (pyorrhea  alveolaris). 

In  view  of  applied  therapeutics  it  is  well  to  consider  these  causes 
separately. 

OVERUSE  OF  TEETH. 

By  overuse  of  a  tooth  is  meant  such  a  variety  of  occlusion  that  the 
tooth  receives  a  greater  stress  than  its  neighbors,  or  than  it  is  designed 
to  bear.  The  stress  may  be  received  in  the  normal  direction,  but  be 
excessive  in  amount.  The  most  prominent  cause  of  this  condition 
is  the  loss  of  one  or  more  other  teeth,  permitting  undue  stress  to  fall 
upon  the  neighboring  teeth,  or,  in  some  cases,  on  far-distant  teeth. 
Too  prominent  artificial  crowns,  particularly  those  of  the  all-gold 
type,  cause  a  general  increase  of  stress  upon  the  pericementum. 
Enormously  overful  contour  fillings  may  establish  a  similar  condition. 
When  but  few  isolated  teeth  remain  in  one  denture  and  have  antag- 
onists, the  teeth  are  certain  to  be  overworked.  Isolated  and  other 
teeth  to  which  are  attached  clasps  of  artificial  dentures  or  too  large 
pieces  of  bridge-work,  are  in  the  majority  of  cases  being  constantly 
overstrained. 

Pathology. — Like  any  other  functional  part  which  is  overworked, 
the  pericementum  is  first  stimulated,  causing  the  vessels  to  dilate. 
Soon  evidences  of  overwork  appear,  and  the  condition  passes  into 


662 


NON-SEPTIC  PERICEMENTITIS 


one  of  interstitial  pericementitis;  the  tooth  projects,  and  is  loosened; 
the  overlying  gum  deepens  in  color,  and  evidences  of  venous  engorge- 
ment are  common  (interstitial  gingivitis).  The  result  of  the  con- 
dition is  a  softening  and  degeneration  of  the  substance  of  the  peri- 
cementum; the  alveolar  wall  is  involved  in  the  degeneration,  and  it 
melts  down — is  resorbed  to  a  greater  or  less  extent.  Cases  have 
been  seen  at  this  point  with  the  gum  margins  as  perfect  as  in  any 
normal   tooth   though   a   symmetrical   resorption   of  margins  may 

Fig.  604 


Illustrating  use  of  overarch  bar.     See  text.     Gorman. ^ 

be  present.  In  one  marked  case  in  which  incisors  met  with  a  slight 
lingual  occlusion  upon  the  lowers,  forcing  them  labially,  the  teeth 
were  as  loose  as  in  the  average  pyorrhea  case,  but  the  gum  margins 
showed  absolutely  no  pocket.  At  any  stage  of  the  disturbance 
marginal  infection  may  occur,  and  the  degeneration  and  destruc- 
tion of  the  pericementum  be  hastened  by  suppuration  or  other 
secondary  degenerations  establishing  pyorrhea  alveolaris. 

The  symptoms,  diagnosis,  and  clinical  history  are  given  in  the 
above  description.     The  prognosis  is  the  inevitable  loss  of  the  tooth 

1  Items  of  Interest,  October,  1913. 


OVERUSE  OF  TEETH 


663 


if  the  causes  be  not  removed,  in  which  event  the  prognosis  is  governed 
b}'  the  extent  to  which  the  degeneration  has  proceeded.  (See 
Interstitial  Gingivitis.)  These  cases  are  often  seen  at  a  time  when 
it  is  difficult  to  say  which  came  first,  the  pyorrhea  or  the  overwork, 
but  the  conditions  of  evident  overstrain,  as  when  posterior  occulsion 
is  largely  lost,  and  the  usually  prompt  response  to  surgical  rest  lead 
to  inference  that  overwork  started  the  predisposition  to  pyorrhea. 
Nevertheless  in  pyorrhea  when  the  marginal  inflammation  has 
caused  bone  resorption  to  the  point  of  tooth  loosening  the  mechanical 
strain  of  occlusion  is  a  cause  of  further  overstrain  and  looseness. 

Fig.  605 


A  case  of  pyorrhea  alveolaris  and  ovL■l■^\"ork.  Five  natural  and  one  artificial  tooth 
mutually  supported  by  holding  against  plate  brace.  Note  restraint  of  right  cuspid 
and  central  by  clasp,  artificial  tooth  bevels  and  T  button  and  restraint  of  left  teeth 
by  clasp  and  button.  This  principle  may  be  employed  in  ordinary  plate  work.  Adap- 
tation made  by  burnishing  thin  pure  metal  to  teeth  model,  and  stiffening  with  solder. 


The  teeth,  if  in  overocclusion,  should  be  dressed  oft"  until  properly 
occluded.  Prosthetic  appliances  should  not  be  so  attached  by  clasps 
as  to  unduly  move  the  clasp  teeth,  especially  buccolingually.  The 
U-clasp  is  worthy  of  consideration  in  this  regard.  The  appliance 
should  support  the  teeth  laterally,  if  possible,  and  occasionally  the 
enclosure  of  the  teeth  by  the  plate  clasps,  with  the  hooks  facing 
each  other  or  a  buccal  embracing  wire  stay,  is  Required,  as,  for 
example,  where  four  lower  bicuspids  only  are  retained  for  support 
to  the  plate,  yet  where  they  also  require  support  (Fig.  617).  Where 
incisors  are  loose  yet  teeth  must  be  inserted  on  plates,  the  judicious 
shaping  of  the  natural  and  artificial  teeth  so  as  to  afford  a  restraint 


664  NON-SEPTIC  PERICEMENTITIS 

of  the  natural  ones  against  the  plate  festoon  is  useful  (Fig.  605). 
In  some  cases  the  festoon  causes  gingivitis  and  tends  to  cause  loosening. 
This  may  be  due  to  an  improper  looseness  of  the  clasps  permitting 
a  rise  and  fall  of  the  plate,  or  the  inner  edge  of  the  festoon  requires 
trimming.  (A  lower  bar  plate  in  which  no  contact  except  at  clasp 
teeth  is  allowed  because  the  bar  lies  beneath  the  tongue  level  and, 
of  course,  away  from  the  teeth  is  an  example  of  the  principle  involved 
in  avoiding  this  class  of  injury).  No  attempt  is  made,  however, 
to  cause  the  artificial  teeth  to  strike  before  the  natural  teeth,  in 
the  hope  of  giving  surgical  rest  to  these  organs.  Such  attempts 
always  result  in  failure,  as  they  cause  injuries  to  the  tissues  upon 
which  the  plate  and  teeth  rest,  which  are  more  severe  than  the 
pericemental  disturbance. 

Properly  adjusted  bridge-work  frequently  does  good  service  in 
these  cases,  provided  the  overoccluding  tooth  or  teeth  be  first  dressed 
down  short  of  occlusion  and  are  given  a  period  of  rest  until  the 
pericementum  recovers.  The  bridge,  if  carefully  planned,  may  be 
made  to  direct  and  control  the  stress  received  by  the  injured  teeth. 
Joining  the  various  bridges  is  useful.  In  this  connection  what  is 
termed  the  "overarch  bar"  is  a  valuable  device.  The  wire  crossing 
the  palate  from  one  bridge  to  another  on  the  opposite  side  automatic- 
ally throws  some  of  the  stress  received  by  the  diseased  teeth  upon 
teeth  upon  the  other  side  of  the  arch,  which  naturally  are  forced  in 
an  opposite  direction  during  mastication  or  at  least  lend  their  support. 
(Fig.  604  illustrates  this.) 

The  use  of  the  Gilmore  attachment  is  useful,  the  wire  supporting 
the  plate  connects  several  teeth  roots  and  gives  them  mutual  support. 

Improperly  occluding  artificial  crowns  should  have  this  fault  cor- 
rected by  removing  the  excess  of  material  or  by  setting  properly 
made  crowns.  All  crowns  should  have  full  mesial  and  distal  contact, 
as  spaces  permit  a  wedging  of  teeth  and  injury  of  the  interdental 
gum  septum,  as  well  as  allow  movement  to  occur. 

Overfull  fillings  should  be  reduced  to  correct  proportions  and 
shape. 

Surgical  rest  is  the  only  hope  of  saving  the  tooth. 

MALOCCLUSION  OF  THE  TEETH. 

Each  tooth  of  a  denture  is  not  only  designed  to  receive  a  definite 
amount  of  force,  but  to  receive  it  in  a  particular  direction  or  direc- 
tions; any  excess  of  this  force,  or  alteration  of  its  direction,  is  followed 
by  abnormal  stimulation  of  the  pericementum  and  by  its  overstrain- 
ing.    The  effects  following  a  general  increase  of  stress  have  been 


MALOCCLUSION  OF  THE  TEETH  665 

considered  under  the  previous  heading.  By  malocclusion  is  here 
meant  the  constant  reception  of  stress  by  the  pericementum  in 
directions  to  which  it  is  quite  unaccustomed,  or  which  are  not  in 
accordance  with  the  anatomical  design  of  the  tooth.  It  is  a  peculiar 
form  of  overuse. 

Causes. — Original  malpositions  of  the  teeth  may  cause  their  faulty 
occlusion.  The  most  prolific  source  of  the  condition  is,  however, 
altered  occlusion  due  to  those  changes  of  position  of  the  teeth  which 
follow  upon  the  loss  of  adjoining  teeth. 

Artificial  crowns,  which  do  not  occlude  in  correspondence  with 
the  other  teeth  are  a  common  cause.  Improperly  formed  fillings 
are  another  cause. 

The  shifting  of  positions  of  the  teeth,  in  consequence  of  patho- 
logical changes  occurring  in  or  about  the  pericementum,  causes  the 
crowns  of  teeth  to  occlude  improperly. 

Pathology. — The  conditions  established  are  those  of  overuse  in  a 
direction  other  than  direct.  A  typical  example  of  this  condition  is 
that  of  a  lower  second  molar  which  has  gradually  tilted  forward  in 
consequence  of  the  loss  of  the  first  molar;  or  a  central  incisor  which 
has  altered  its  position  in  consequence  of  secondary  formations  in 
or  about  the  pericementum,  a  common  precursor  of  phagedenic 
pericementitis.  Some  portion  of  the  tooth,  an  edge,  which  before 
did  not  occlude  with  an  antagonizing  tooth,  is  brought  into  occlu- 
sion; if  the  occlusion  be  not  unduly  forcible,  no  immediate  degenera- 
tive changes  are  evident.  If  the  occlusion  be  excessive,  the  peri- 
cementum is  not  uniformly  affected,  but  the  greatest  stress  is  brought 
to  bear  upon  some  lateral  aspect  of  the  structure.  It  responds 
in  the  degree  of  the  overwork,  and  inflammation  and  degenerative 
changes  occur,  which,  if  the  active  causes  be  not  removed,  gradually 
spread  to  other  portions  of  the  pericementum,  and  the  phenomena 
noted  in  connection  with  overuse  occur,  but  are  not  so  general  in 
distribution.  The  tooth  becomes  more  movable  in  one  or  more 
directions — i.  e.,  is  loosened;  it  may  develop  some  degree  of  tender- 
ness upon  percussion,  and  the  gum  color  toward  the  affected  side 
deepens,  although  it  may  remain  normal  in  other  parts.  As  in  the 
previous  cases,  infection  may — indeed,  is  likely  to — occur.  In 
some  cases  the  pericementum  may  degenerate  and  be  destroyed 
about  one  root  of  a  multirooted  tooth,  and  remain  about  the  other. 
It  is  to  be  remembered  that  a  less  degree  of  irritation  may  produce 
hypercementosis. 

Pyorrhea  alveolaris  in  any  form  is  a  localized  suppurative  peri- 
cemental inflammation,  which  causes  inflammation  of  the  peri- 
cementum in  general.      Swelling  occurs  and  the  tooth  is  pushed  up 


666  NON-SEPTIC  PERICEMENTITIS 

into  malocclusion.  Other  teeth  are  sometimes  urged  out  of  occlu- 
sion by  these.  Such  teeth  may  sometimes  be  dressed  off  one  thirty- 
second  of  an  inch  before  the  overocclusion  is  relieved.  A  direct 
result  of  the  strain  and  compression  brought  to  bear  upon  apical 
tissue  is  the  production  of  non-septic  pulpitis  with  reflex  pain  and 
response  to  heat  and  cold  (see  Fig.  413). 

Diagnosis  and  Treatment. — In  all  malposed  teeth  a  careful  examina- 
tion should  be  made  of  their  mode  of  occlusion.  If  the  tooth  exhibit 
tenderness  and  looseness,  malocclusion  is  almost  a  certainty;  it  only 
remains  to  determine  its  direction. 

The  spots  of  faulty  occlusion  may  be  determined  by  placing  a 
strip  of  carbon  paper  (articulating  paper)  over  the  tips  of  the  antag- 
onizing teeth  and  having  the  patient  bite;  the  spots  of  contact  should 
then  be  ground  away  until  the  tooth  is  slightly  short  of  direct  occlu- 
sion. Fresh  strips  of  paper  are  used,  and  the  jaws  moved  laterally, 
as  in  mastication,  to  note  other  points  of  contact;  these  should  also 
be  ground  away. 

It  suffices  in  some  acute  cases  to  place  a  rubber  dam  or  metal  cap 
guard  upon  a  nearby  tooth  for  a  day  or  two  to  prevent  occlusion 
upon  the  sore  tooth,  which  regains  its  normal  position  in  the  alveolus 
as  the  inflammation  subsides.  The  grinding  and  guarding  may  be 
combined,  judgment  being  required. 

Prognosis. — If  the  condition  be  not  corrected  every  time  occasion 
requires,  the  degeneration  progresses  until  the  tooth  is  lost. 

If  marginal  infection  has  occurred,  purulent  or  non-purulent 
marginal  pericemental  liquefaction  (pyorrhea  alveolaris)  may  have 
to  be  considered. 

DISUSE  OF  TEETH. 

Definition. — By  disuse  of  teeth  is  meant  a  degree  of  usage  less  than 
the  amount  which  the  forms  and  structure  of  the  teeth  and  contiguous 
parts  fit  them  for.  The  disuse  may  be  absolute  or  relative;  teeth 
may  not  occlude  at  all,  owing  to  the  loss  of  antagonists  or  to  extremely 
irregular  positions. 

Partial  Disuse. — Causes  and  Pathology. — If  soft  food  be  used 
instead  of  that  requiring  vigorous  mastication,  or  if  one  tooth  of  a 
side  be  diseased  so  that  that  side  of  the  mouth  is  unused  in  mastica- 
tion, or  if  one  of  the  antagonists  of  a  tooth  be  lost,  the  pericementi 
of  the  teeth  involved  do  not  receive  their  proper  amount  of  exercise, 
and  a  degree  of  atony  ensues. 

This  partial  disuse  has  a  more  distinct  relation  to  the  health  of  the 
gum  margin,  which  does  not  receive  a  normal  amount  of  friction 


DISUSE  OF  TEETH  667 

from  mastication,  and  if  this  be  not  oflFset,  in  part,  by  prophylaxis, 
marginal  gingivitis  ensues. 

Infection  and  the  formation  of  calculus  increase  the  irritation  to  a 
marginal  gum  inflammation,  which  is  liable  to  run  into  a  pyorrhea 
alveolaris.     This  is  the  real  significance  of  disuse  as  a  cause. 

Diagnosis  and  Prognosis. — A  diagnosis  of  disuse  (relative)  is  usually 
made  out  by  inquiring  as  to  the  food  habit  of  individuals.  It  is 
excessively  common  in  civilized  communities,  particularly  among 
the  well-to-do,  and  is  of  almost  constant  occurrence  in  gourmands. 

Treatment. — Patients  should  have  pointed  out  to  them  the  results 
of  insufficient  mastication,  together  with  the  evils  of  faulty  oral 
hygiene.  Every  effort  should  be  made,  by  the  use  of  constant 
prophylactic  measures,  to  forestall  the  occurrence  of  pyorrhea 
alveolaris.  This  and  similar  conditions  are  particularly  to  be  feared 
in  the  degenerative  periods  of  early  and  late  middle  age.  It  is 
between  the  ages  of  thirty  and  fifty  years  that  ill-consequences 
are  most  to  be  feared  from  acquired  debility  of  the  pericementum. 

Absolute  Disuse. — Teeth  which  perform  no  work  directly  in  masti- 
cation, or  indirectly  by  serving  as  abutments  for  a  bridge-piece, 
may  be  said  to  be  in  a  condition  of  absolute  disuse. 

Results, — A  tooth  or  root  whose  pericementum  receives  no  stimulus 
becomes  relatively  a  foreign  body  to  the  organism.  It  is  a  useless 
part,  and  the  body  attempts  to  cast  it  out.  Perhaps  these  phrases 
are  insufficiently  exact;  however,  a  disused  tooth  is  lost  through  a 
series  of  pathological  changes.  It  is  probable  that  the  impact  of 
blood  pressure  raises  the  tooth  an  infinitesimal  distance,  and  being 
without  antagonism  it  does  not  wholly  recover  its  normal  position. 
The  aggregate  of  these  infinitesimal  differentials  being  expressed  in 
protrusions,  probably  lack  of  accustomed  pressure  allows  a  slight 
overfulness  of  blood  with  further  increased  blood  pressure  (see  p. 
123).    Devitalization  of  the  pulp  sometimes  lessens  this. 

This  is  a  fairly  rapid  process,  and  occurs  often  after  the  trim- 
ming of  teeth  for  bridge-work  so  as  to  interfere  with  the  planned 
occlusion,  unless  the  bridge  be  rapidly  made.  If  unopposed,  it 
extends  progressively,  the  neck  being  usually  exposed,  though  some- 
times the  alveolar  process  becomes  developed  and  lies  on  a  lower 
level  as  though  it  had  followed  the  tooth  down.  Usually  the  bifur- 
cation of  a  molar  becomes  exposed,  calculi  form,  and  the  extrusion 
becomes  hastened  by  marginal  gingivitis.  The  tooth  may  be  firm 
even  though  half  its  root  length  be  exposed,  though  often  it  becomes 
looser  than  normal.  Sometimes  it  strikes  other  teeth  with  a  glancing 
motion.  If  the  teeth  in  Fig.  606  were  closer  this  would  occur,  and 
such  a  process  (malocclusion)  hastens  the  loosening.     The  opposite 


668  NON-SEPTIC  PERICEMENTITIS 

gum  may  be  injured  by  such  a  tooth.  Another  effect  is  the  wedging 
of  food  between  the  teeth  owing  to  a  favoring  entrance,  the  laterally 
unsupported  tooth  wedging  apart  and  then  closing  upon  the  food. 
This  injures  the  gum  septum.     (See  Gingivitis.) 

Finally  the  loosening  or  the  annoyance  compels  the  removal  of 
the  tooth. 

The  danger  of  marginal  infection  is  always  great  in  these  cases. 
Some  degree  of  infection,  no  doubt,  exists  in  all  of  them,  which 
serves  to  explain  the  increased  rapidity  of  the  degenerations. 

Fig.  606 


Absolute  disuse  and  elongation  of  an  upper  and  a  lower  molar;  partial  disuse  of 
bicuspid;  small  abscess  cavity  in  the  bone  about  a  root.  (Philadelphia  Dental 
College  Museum.) 

Prognosis. — If  teeth  can  be  directly  or  indirectly  brought  into  use, 
so  that  their  pericementi  receive  exercise,  the  cases  may  recover, 
provided  the  atrophic  changes  are  not  very  pronounced;  in  which 
event  the  atrophy  proceeds,  although  more  slowly.  Teeth  crowned 
or  made  abutments  for  bridges,  after  degenerative  changes  have 
become  established — i.  e.,  when  the  normal  pericementum  has  been 
replaced  by  a  thickened  mass  of  partially  organized  connective  tissue 
— usually  become  progressively  looser;  the  alveolar  atrophy  proceeds 
until  all  attachment  is  lost. 

If  this  principle  be  utilized  early,  the  teeth  may  be  saved.  The 
results  are  better  if  the  teeth  or  roots  be  utilized  before  the  age  of 
thirty  than  at  later  ages. 

Treatment. — The  treatment  consists  in  bringing  the  teeth  into  use, 
if  the  degeneration  has  not  proceeded  too  far.  In  crowning  for  a 
bridge  pier  it  is  customary  to  shorten  the  crown  to  the  general  occlusal 


FIBROID  DEGENERATION  OF  THE  PERICEMENTUM      669 

level,  though  even  if  a  little  longer  and  not  in  direct  occlusion  the 
tooth  is  brought  into  a  sort  of  mastication  which  is  useful  if  it  does 
not  introduce  an  element  of  malocclusion,  i.  e.,  if  the  distal  or  repelling 
strain  upon  its  mesial  slope  is  compensated  for  by  the  mesial  strain 
upon  a  pier  or  piers  more  mesial  to  it,  or  upon  a  pontic  tooth,  for 
example,  upon  the  cuspid  of  Fig.  606,  or  pontic  bicuspid  occluding 
with  the  mesial  slope  of  the  lower  first  molar.  In  such  a  case  as  this 
grinding  both  the  upper  and  lower  molar  occlusally  and  the  intro- 
duction of  an  upper  bridge  is  indicated.  Later,  extraction  is  inevit- 
able. The  operation,  when  determined  upon,  should  not  be  delayed, 
for  not  only  are  bacterial  growths  invited  about  the  loosened  tooth, 
but  the  soft  tissues  are  frequently  increased  in  volume,  and  if  extrac- 
tion be  delayed  until  complete  local  atrophy  of  the  alveolar  walls 
has  taken  place,  a  soft  and  spongy  mass  remains,  which  interferes 
with  the  comfortable  wearing  of  prosthetic  appliances  in  the  future. 

FIBROID  DEGENERATION  OF  THE  PERICEMENTUM. 

Fibroid  degeneration  of  the  pericementum  is  a  senile  atrophic 
change  occurring  in  teeth,  the  pericementi  of  which  have  run  a 
healthy  life  course,  but  finally  have  become  subject  to  senile  marantic 
constitutional  changes  of  not  clear  nature.  The  condition  thus  first 
defined  by  Hopewell-Smith^  is  further  described  as  found  in  that 
class  of  teeth  of  the  aged  which  have  resorbed  alveolar  margins  and 
exposed  cementum,  but  not  necessarily  subject  to  pyorrhea  alveo- 
laris,  though  traumatic  pericementitis  may  be  present.  In  some 
cases  the  teeth  may  be  firm. 

Pathohistology. — The  chief  characteristics  are  an  increase  in  size 
of  the  fibers  of  the  pericementum,  the  loss  of  their  nuclei,  their 
generally  structureless  character,  and  their  arrangement  in  promi- 
nent bundles  about  large  spaces  (areolae).     (See  Fig.  607.) 

The  fibers  are  firmly  implanted  in  both  bone  and  cementum.  The 
cementum  does  not  become  hyperplastic  (hypercementosed),  but 
the  bone  becomes  osteoporous  and  the  Haversian  canals  contain  a 
shrunken. fibroid  tissue  resembling  that  in  the  pericementum  (Fig. 
608). 

The  gum  tissue  in  the  vicinity  also  undergoes  retrogressive  changes 
in  sympathy,  becomes  less  vascular  and  more  fibroid. 

The  condition  may  persist  without  inflammatory  or  suppurative 
changes,  though  it  may  act  as  a  cause  of  obscure  neuralgia  or  as  a 
predisposing  cause  to  pyorrhea  alveolaris. 

1  Dental  Cosmos,  1904. 


Fig.  607 


Fibroid  degeneration  of  the  pericementum:     C,  cementum;    A,  alveolus;    F,  fibers 
with  decrepit  nuclei.    Transverse  section.     (Hopewell-Smith.) 


Fig.  608 


A  __  -X 


H 


M 


Fibroid  degeneration  of  the  pericementum:  C,  cementum;  M,  degenerated  peri- 
cementum; A,  alveolus;  H,  enlarged  (osteoporous)  Haversian  canals.  Transverse 
section.     (Hopewell-Smith.) 


ACCIDENTS  TO   TEETH  671 

Hopewell-Smith  points  out  that  the  areolar  spaces  may  admit 
microorganisms  to  deep  parts,  thus  predisposing  to  antral  disease  or, 
possibly,  osteomyelitis. 

ACCIDENTS  TO  TEETH. 

Apart  from  fracture  of  the  teeth  by  accident,  several  interesting 
accidental  conditions  involving  therapeutics  require  consideration. 

Teeth  Driven  into  Alveolar  Process. — Blows,  falls,  etc.,  have  occasion- 
ally caused  teeth  to  be  driven  forcibly  into  the  jaw.  The  condition 
may  be  complicated  by  fracture,  in  which  case  the  judgment  of 
the  operator  must  be  exercised.  If  the  tooth  be  not  fractured 
it  may  be  drawn  down  with  forceps  and  ligated  in  place  until  firm. 
The  use  of  zinc  phosphate  upon  the  ligatures,  if  possible  to  use  it, 
renders  them  more  rigid.  Splints  may  be  used.  If  evidence  of  pulp 
death  be  noted  by  subsequent  test,  or  apical  pericemental  inflam- 
mation, the  pulp  should  be  removed. 

Luxation  or  Partial  Dislocation  by  Accident. — Teeth  may  be  par- 
tially knocked  out  and  driven  either  lingually  or  buccally.  The  pulp 
connections  will  be  ruptured,  as  a  rule,  but  after  asepsis  of  the  parts 
by  means  of  antiseptic  sprays  the  teeth  may  be  pressed  into  place, 
and  if  ligated  or  splinted  may  again  become  firm  by  deposition  of 
bone  about  them.  The  pulps  nearly  always  give  evidence  of  death 
so  that  they  should  be  later  replaced  by  canal  fillings. 

Mendel  Joseph  and  Dassonville^  record  experiments  on  dogs 
showing  a  vital  attachment  of  the  pulp  of  an  immediately  replanted 
tooth.     They  used  strictly  aseptic  precautions. 

Occasionally  evidences  of  reattachment  of  pulp  have  been  recorded^ 
even  after  total  displacement.  If  the  accident  result  in  elongation 
of  the  tooth  with  production  of  a  chronically  spongy  pericementum, 
the  operation  of  replantation  should  be  performed. 

Total  Dislocation  of  Teeth  by  Accident. — If  the  accident  result 
in  total  displacement  from  the  mouth,  the  tooth  or  teeth  may  be 
prepared  as  for  replantation  (see  p.  624),  and  under  aseptic  pre- 
cautions replanted  in  their  alveoli.  If  held  by  ligatures  or  splints 
they  will  usually  become  firm.  If  the  teeth  are  kept  moist  a  short 
delay  if  necessary  does  not  prevent  success,  though  clot  and  granula- 
tions must  be  swept  out. 

Attachment  of  Teeth. — -Two  or  more  teeth  may  be  attached  by  the 
intervening  alveolar  process,  fracture  of  which  may  cause  both  teeth 
to  be  removed  in  extraction.     In  a  few  cases  of  loose  deciduous  teeth 

1  L'Odontologie.     See  Dental  Cosmos,  1906,  p.  1060. 

2  Kirk  and  W.  Trueman. 


672  NON-SEPTIC  PERICEMENTITIS 

the  gum  has  been  sufficient  attachment  to  cause  the  removal  of  two 
teeth  at  once. 

In  some  cases  the  tough,  fibrous  nature  of  the  pericementum 
causes  the  alveolar  bone  fractured  by  the  leverage  upon  it  to  remain 
attached  to  the  tooth,  and  Fig.  210  illustrates  teeth  attached  by 
union  of  pericementum  only. 

Fracture  of  the  Alveolar  Process.^ — Slight  fractures  of  the  alveolar 
plate  are  of  little  consequence,  as  a  rule.  In  some  cases  one  plate 
may  be  fractured,  and  unless  removed  with  the  tooth,  may  usually 
be  pressed  back  into  place.  Reunion  may  be  looked  for  if  asepsis 
be  maintained.  Fractures  of  the  alveolar  process  from  blows, 
kicks,  etc.,  upon  the  jaw  may  become  septic  and  sequestra  may 
form,  necessitating  removal  of  both  bone  and  teeth.  Such  fractures 
should  have  immediate  attention.  Fractures  of  the  maxillae  should, 
of  course,  be  immediately  reduced. 

Hemorrhage  following  Extraction. — Even  in  the  absence  of  hem- 
ophilia postextraction  hemorrhage  may  be  somewhat  severe,  and 
is  well  controlled  by  a  little  tannic  acid  or  powdered  alum  and  thymol 
upon  a  pellet  of  cotton,  or  nosophen  gauze  wet  with  phenolsodique. 

If  necessary  a  linen  compress  should  be  placed  over  it  and  a  Barton 
or  Garretson  bandage  applied.  The  internal  use  of  calcium  chlorid 
or  other  hemostatic  is  indicated  if  the  bleeding  be  continued.  (See 
p.  120.) 

Lacerations. — The  tongue,  floor  of  the  mouth,  etc.,  may  be  lacer- 
ated by  the  careless  use  of  forceps,  and  the  lacerated  parts  should 
be  irrigated  with  antiseptics  and  the  mouth  kept  under  astringent 
antiseptics  while  the  parts  are  healing.  Lacerated  gum  margins 
should  be  trimmed  up  to  prevent  sloughing. 

Postextraction  Alveolitis. — This  has  been  already  discussed.  (See 
p.  633.) 

For  ordinary  transient  pain,  phenolcamphor  with  or  without 
menthol  added  or  equal  parts  of  phenolsodique  and  laudanum  are 
useful.  Hot  salt  water  held  in  the  mouth  is  analgesic,  styptic  and 
stimulant. 


SECTION  VI. 

PERICEMENTAL   DISEASES  BEGINNING   AT 
THE   GUM   MARGIN. 


CHAPTER  XXII. 
GINGIVITIS. 

The  diseases  which  begin  at  the  gum  margin  are  all  inflammatory, 
and  are  due  to  mechanical,  chemical,  and  infective  local  irritants, 
and  probably  may  be  due  to  overexcitation  of  the  gum  tissues  by 
leukomains  or  other  toxic  products  which  are  formed  intrinsically 
within  the  body  in  malnutritional  processes,  also  to  overexcitation 
by  certain  drugs,  both  of  which  the  gum  is  endeavoring  to  eliminate. 
The  inflammation  resulting  is  termed  gingivitis.  Many  mechanical 
or  septic  causes  which  produce  pericementitis,  such  as  overuse  or 
apical  abscess,  finally  induce  an  inflammation  in  the  alveolar  bone 
(osteitis),  and  later  an  inflammation  of  the  gingival  tissue.  In 
reverse  order,  inflammations  beginning  in  the  gum,  reach  the  bone, 
and  later  the  pericementum.  It  is  plain  then  that  pericementitis  and 
gingivitis  are  often  associated,  and  at  the  gum  margin  are  almost 
inseparable. 

If  at  any  stage  of  a  gingivitis,  whether  of  mechanical  or  chemical 
primary  causation,  infection  enter  the  inflammation  becomes  septic, 
and  if  pyogenic  bacteria  are  the  infective  agents,  pus  is  formed.  At 
this  juncture  there  is  a  pus  flow  from  beneath  the  gum  margin, 
usually  from  a  pocket  extending  into  the  substance  of  the  perice- 
mentum or  the  location  previously  occupied  by  it  in  the  alveolus, 
and  from  this  fact  it  is  called  pyorrhea  alveolaris,  though  a  variety 
of  pyorrhea  is  apparently  non-purulent.  Some  writers  treat  of  all 
cases  of  gingivitis  as  cases  of  pyorrhea,  advanced  or  incipient,  and 
in  view  of  the  fact  that  a  simple  gingivitis  may  become  a  pyorrhea 
there  is  some  justification  from  a  preventive  standpoint;  nevertheless, 
there  are  so  many  phases  of  gingivitis  that  for  purposes  of  discussion 
and  applied  therapeutics  it  is  advisable  to  specify  the  various  forms 
that  may  exist. 

43  (673) 


674     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

If  confined  to  the  gum  margin  it  is  properly  designated  marginal 
gingivitis;  if  the  inflammatory  elements  (leukocytes  and  exudates) 
have  infiltrated  the  deeper  connective  tissues  it  may  be  called  deeply 
seated  gingivitis  or  interstitial  gingivitis.  If  a  pus  flow  from  the 
alveolus  accompany  the  deeply  seated  gingivitis  the  condition  of 
pyorrhea  alveolaris  is  established. 

With  any  of  these  conditions  an  hypertrophy  or  an  atrophy  may 
be  associated,  which,  on  the  one  hand,  may  result  in  hypercementosis 
or  exostosis  or  thickening  of  gum,  or,  on  the  other,  in  resorption  of 
gum  or  bone. 

MARGINAL  GINGIVITIS. 

Definition. — By  marginal  gingivitis  is  meant  an  inflammation  con- 
fined to  the  margins  of  the  gums  about  the  necks  of  the  teeth. 

Causes. — The  causes  of  marginal  gingivitis  are  local  and  general, 
which  may  be  subdivided  into  predisposing  and  exciting.  Both 
local  and  general  causes  may  be  in  action  at  the  same  time. 

Local  Causes. — Marginal  gingivitis  may  be  excited  by  the  pres- 
ence of  food  masses  or  unremoved  collections  about  the  necks  of 
teeth,  their  fermentation  liberating  chemical  products  more  or  less 
irritating.  Miller^  has  shown  that  the  materies  alba  about  the  necks 
of  teeth  may  have  either  an  alkaline  or  acid  reaction,  and  the  gums 
be  inflamed. 

The  lack  of  contact  or  too  light  contact  of  approximal  surfaces, 
whether  due  to  faulty  operations  or  induced  by  the  wedging  action 
of  tooth-picks  or  floss  silk,  causing  a  general  non-septic  pericementitis 
and  bone  resorption  (looseness  of  teeth)  are  contributory  to  the 
wedging  of  food. 

Bacterial  plaques  not  unlike  those  producing  dental  caries  have 
been  shown  by  Miller^  to  be  formed  upon  many  surfaces  of  the  teeth 
even  when  no  ill  results  are  notable.  In  practice  staining  the  teeth 
with  tincture  of  iodin  will  readily  demonstrate  the  presence  of  such 
bacterial  films.  Under  favoring  circumstances  these  no  doubt 
produce  marginal  gum  irritation,  a  fact  proved  by  the  relief  of  such 
a  condition  by  prophylaxis — i.  e.,  the  removal  of  the  plaques. 

Talbot^  has  demonstrated  that  a  deep  pocket  may  normally  exist 
at  the  gum  margin  favoring  the  retention  of  food  and  other  debris. 

Mechanical  causes  produce  direct  irritation;  these  are  deposits  of 
salivary  calculus  resting  upon  the  gum  or  beneath  the  gum  margin; 
fillings  projecting  beyond  cavity  margin;  edges  of  poorly  fitted  crown 
band  and  the  putrefaction  of  food,  etc.,  collected  in  the  places  from 

1  Dental  Cosmos,  1894.  2  ibid,  1902. 

'  Intestitial  Gingivitis. 


MARGINAL  GINGIVITIS  675 

which  cement  has  washed  out;  gum  overlying  cavity  margins;  bruising 
of  the  gum  margin  by  food  crowded  between  teeth  and  removed 
by  toothpicks;  the  fermentation  of  such  crowded  food  (see  p.  683); 
the  mechanical  action  of  toothpicks  or  floss  silk  improperly  crowded 
upon  the  gum  margin;  projecting  edges  of  artificial  crowns  or  bits 
of  cement  used  in  their  cementation ;  toothbrush  bristles ;  fragments 
of  toothpicks,  bones,  or  oyster-shells,  etc. ;  rings  of  rubber  or  of  torn 
rubber  dam  or  ligatures  left  in  position;  rubber  or  tape  wedges 
forced  into  the  gum;  the  crowding  back  of  a  gum  by  ligation 
which  produces  ischemia  for  hours;  improper  contact  of  the  edges 
of  prosthetic  plates  or  appliances  about  the  necks  of  teeth;  injuries 
inflicted  by  rubber  dam  clamps,  wedges,  ligatures,  etc.;  the  eruption 
of  teeth  through  the  gums. 

An  interesting  case  of  recurrent  epileptic  attacks  was  proved  due 
to  a  toothbrush  bristle  forced  into  the  gum.^ 

The  action  of  any  of  these  causes  may  be  complicated  through 
the  infection  of  the  mechanically  irritated  part  by  oral  bacteria. 
An  excellent  example  occurred  in  the  editor's  practice.  A  perfect 
gum  margin  was  irritated  by  the  margins  of  a  gutta-percha  cap 
used  as  a  remedy  for  hyperemia  of  the  pulp.  Pyogenic  organisms 
produced  a  marginal  suppuration  which  subsided  upon  removal  of 
the  cap. 

All  forms  of  marginal  gingivitis  are  to  be  considered  as  incipient 
inflammations  which,  let  alone,  may  lead  to  deep-seated  inflammation 
and  tissue  destructions  collectively  called  pyorrhea  alveolaris. 

Excessive  smoking  and  the  use  of  alcoholic  liquors  produce  local 
irritative  effects,  resulting  in  catarrhal  stomatitis  and  gingivitis. 

Lack  of  exercise  or  brushing  of  the  gums  produces  an  atonic 
condition  of  the  gum  margin,  predisposing  to  gingivitis  of  infective 
character.  Too  persistent  brushing  with  stiff  brushes  may  be 
equally  injurious  by  causing  marginal  irritation. 

A  variety  of  ulcerative  marginal  gingivitis  exists  which  tends  to 
rapidly  penetrate  the  pericemental  tissue  and  may  cause  pyorrhea. 
The  gum  margin  has  a  pasty,  sloughing  appearance,  and  the  gum 
about  several  teeth  may  be  involved.  Vaughn^  describes  it  as 
covered  by  a  grayish  necrotic  covering  which  when  rubbed  off  leaves 
a  sensitive  bleeding  surface,  the  deposit  being  accumulated  rapidly 
in  an  hour  or  two.  He  found  the  bacillus  fusiformis  and  spirillum 
which  work  in  symbiosis  in  Vincent's  angina.  In  the  severe  cases 
he  describes  fever,  dysphegia,  headache,  malaise,  nausea,  marked 
salivation,  loss  of  appetite,  increased  cardiac  and  respiratory  action, 

1  Dental  Cosmos,  1910,  p.  594.  =  Ibid.,  1912,  p.  651. 


676     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

and  glandular  enlargement  as  associate  phenomena.  The  breath  is 
offensive  and  characteristic.  Syphilitic  chancre  may  begin  at  the 
gum  margin,  and  there  is  no  reason  why  aphthae  should  not  be  so 
located  though  usually  elsewhere. 

A  form  of  phagedenic  pericementitis  causing  very  rapid  destruc- 
tion of  the  pericementum  and  loss  of  the  teeth  without  loss  of  alveolar 
wall  has  occasionally  been  noted.  In  one  notable  case  two  upper 
incisors  came  away  three  weeks  after  an  ulceration  appeared  about 
their  gum  margins.  The  patient  wore  the  teeth  for  several  weeks 
in  situ,  and  could  remove  and  reinsert  them  at  will.  The  alveolar 
walls  were  bare,  but  intact.  There  was  but  little  pain.  The  sockets 
healed  after  removal  of  the  teeth  and  the  freshening  of  the  bone. 
The  clinical  features  of  this  case  were  entirely  distinct  from  those 
of  the  phagedenic  condition  recognized  as  phagedenic  pericementitis, 
and  were  more  probably  caused  by  the  Vincent  bacteria  (Fig.  611). 

Cook  has  shown  that  stimulant  and  astringent  washes,  if  used 
to  excess,  have  a  degenerative  influence  upon  the  gum  margin.  (See 
p.  84.)     A  too  powerful  formaldehj'^d  wash  has  the  same  effect. 

The  production  of  deeply  seated  gingivitis  by  causes  of  systemic 
or  drug  origin  involves  a  marginal  gingivitis,  but  marginal  gingivitis 
is  not  always  produced  by  local  causes  of  interstitial  gingivitis;  at 
least,  not  at  first  (see  p.  648). 

Systemic  Causes. — These  are  the  same  as  for  Deeply  Seated  Gingi- 
vitis, which  see. 

Pathology. — The  pathology  of  marginal  gingivitis  is  that  of  an 
inflammation  located  in  a  peculiar  situation — i.  e.,  in  the  marginal 
gum  tissue — and  tending  to  spread  into  the  deeper  interstitial  tissues. 
(See  Pathology  of  Deeply  Seated  Gingivitis.)  As  shown  above 
when  pyogenic  bacteria  enter,  a  pus  flow  or  pyorrhea  is  established. 

Symptoms. — The  symptoms  of  marginal  gingivitis  depend  upon  the 
cause  and  degree  of  inflammatory  action.  When  mechanical 
causes  are  acting  the  gum  presents  an  inflamed  appearance;  it  is 
swollen,  of  a  bright  red  or  purplish  color,  very  sensitive  to  touch, 
and  bleeds  readily. 

If  a  calculus  rest  against  the  gum,  the  latter  may  present  a  raw, 
chronically  inflamed  surface  in  contact  with  it.  A  ragged,  red, 
split  margin  of  gum  is  often  associated  with  calculus  upon  the  labial 
surfaces  of  lower  incisors,  cuspids,  and  bicuspids,  and  upper  cuspids 
and  bicuspids.  At  times  the  lingual  surfaces  of  the  lower  incisors 
present  such  an  appearance.  If  subgingival  calculus  be  present, 
the  gum  margin,  if  markedly  affected,  appears  loosened,  and  is  of 
a  flabby  appearance  and  purplish  in  color.  In  some  cases  the  gum 
margin  appears  thickened  or  hj^pertrophied. 


MARGINAL  GINGIVITIS  677 

A  bloodshot  appearance — i.  e.,  enlargement  of  terminal  vessels — 
is  often  seen  in  gingivitis. 

In  cases  due  to  unhygienic  conditions — i.  e.,  food  collections  or 
vitiated  secretions  about  the  necks  of  teeth — a  raw,  red,  outer 
surface  of  the  gum  margin  is  noted,  particularly  in  young  persons. 

In  stomatitis  ulcerosa  a  yellow,  pasty  ulceration  of  the  gum  mar- 
gins may  occur.  It  is  rodent  in  character,  very  painful,  and  may 
cause  rapid  loss  of  the  pericementum  and  of  the  tooth.  (See  Vincent's 
Angina  and  p.  681.)  In  gingivitis  due  to  oral  infection  by  the  coccus 
of  gonorrhea  an  intense  gingival  inflammation  with  looseness  of 
the  teeth,  pyorrhea  alveolaris,  and  profuse  salivation,  may  occur.^ 

Talbot^  describes  a  greenish-gray  glazed  surface  of  ulcerated 
raw  gum  in  two  cases  of  profuse  interstitial  gingivitis  due  to  the 
gonococcus. 

Stein  is  inclined  to  doubt  the  etiology.^ 

The  calssification  of  the  gingivitis  depends  upon  the  cause  and 
progress  of  the  disease. 

Prognosis. — If  the  case  has  run  an  acute  course  and  is  due  to  the 
action  of  mechanical  causes  plus  infection,  recovery  is  usually  prompt 
upon  the  removal  of  the  cause  and  sterilization  of  the  injured  part. 
In  the  chronic  cases  due  to  the  more  slowly  acting  mechanical  and 
infective  causes  combined — e.  g.,  salivary  calculus  plus  infection 
— much  deeply  seated  gingivitis  may  have  occurred  accompanied 
by  pericemental  and  alveolar  resorption.  This  usually  constitutes 
a  permanent  loss.  If  the  gum  margin  is  in  a  state  of  atony  or  inflam- 
mation as  the  result  of  collections  of  bacteria,  etc.,  upon  the  cervices 
of  the  teeth,  their  condition  may  be  improved  by  frequent  prophy- 
laxis. 

Treatment. — The  treatment  of  the  condition  consists  in  removing 
the  source  of  irritation  and  restoring  the  normal  circulation  in  the 
parts.  If  the  source  of  the  disorder  be  in  some  underlying  constitu- 
tional condition,  the  symptoms  may  be  ameliorated,  although  not 
entirely  cured,  by  the  correction  of  the  general  disorder. 

Cases  due  to  mechanical  irritation  are  commonly  confined  to  one 
or  several  teeth,  rarely  to  an  entire  denture,  except  cases  continued 
in  consequence  of  deposits  of  scaly  calculi  beneath  the  gum  margin 
or  under  plates.  Foreign  bodies,  such  as  bristles  and  fragments  of 
bone,  should  be  removed.  Projecting  fillings  or  overhanging  crown 
margins  should  be  made  flush  with  the  general  tooth  surface.     Sali- 

1  Vines.    British  Journal  of  Dental  Sciences,  1903,  and  Dental  Cosmos,  1903. 
-  Dental  Cosmos,  1905. 

3  Bacteriology  in  its  Relationship  to  the  Oral  and  Nasal  Cavities.  Items  of  Interest, 
1914. 


678     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

vary  calculi  should  be  removed.  When  food  crowds  upon  gum 
margins  between  teeth,  lateral  or  mesiodistal  contacts  should  be 
established  either  by  contouring  filling,  introducing  a  bridge  which 
establishes  such  proximal  contact,  or  in  some  cases  by  wedging  at 
some  convenient  point  so  as  to  crowd  several  teeth  together,  then 
introducing  a  contour  filling  or  inlay.  The  contact  should  exist 
just  a  little  to  the  gingival  of  the  marginal  ridges  and  not  be  too  broad 
and  should  be  well  rounded. 

In  another  phase  of  this  condition  in  the  WTiter's  own  mouth  the 
extraction  of  a  lower  third  molar  allowed  the  distal  cusp  of  the 
lower  second  molar  to  wedge  between  the  upper  second  and  third 
molars,  so  that  the  third  molar  was  pushed  distally  and  shredded 
food  packed  in  simultaneously  causing  extreme  and  annoying  gingi- 
vitis. In  such  a  case  if  grinding  the  cusps  of  the  antagonizing 
molars  does  not  relieve,  only  extraction  or  firm  attachment  of  the 
third  and  second  molar  will  give  relief  (Fig.  609).  In  a  few  similar 
cases  where  fillings  were  present  the  fillings  have  been  overcontoured 
and  an  iridio-platinum  w^re  imbedded  in  a  groove  in  one  filling 
and  the  other  pointed  end  allowed  to  rest  in  a  slight  groove  in  the 
adjoining  filling.  In  this  it  plays  freely  but  prevents  the  crowding 
of  food,  though  food  may  float  in  laterally  without  direct  injury. 

Fig.  609 


Marginal  gingivitis  located  in  septal  tissue  between  upper  second  and  third  molar 
(see  text).  Also  shows  anterior  drifting  of  second  molar,  due  to  extraction  of  first 
molar  early  in  life. 


This  condition  frequently  results  when  a  bridge  has  been  inserted 
from  a  second  molar  forward.  The  third  molar  moves  away.  If 
any  looseness  of  teeth  exist  it  may  be  better  to  include  the  third 
molar  as  an  abutment. 

A  further  possibility  lies  in  the  use  of  a  crown  on  the  third  molar 
with  a  hook  or  mortised  piece  attached,  which  hook  or  mortise  plays 
in  a  suitable  pocket  in  the  crown  attached  to  the  bridge,  or  the  pin 


MARGINAL  GINGIVITIS 


679 


referred  to  may  play  in  a  groove.  Some  cases  of  bridge  work  are 
constructed  with  hook  attachment,  said  hook  playing  in  a  specially 
made  inlay  in  a  tooth  not  otherwise  included  in  the  bridge  (Fig. 
610). 


Fk;.  010 


Pin  embedded  in  filling  in  third  molar  and  extending  into  a  groove  in  filling  in 
second  molar.     Extension  plays  back  and  forth  but  protects  gum. 


Any  associate  pyorrhea  due  to  this  cause  is  usually  rapidly  cured 
by  this  establishment  of  contact. 

Following  this,  perfect  cleansing  of  all  teeth  is  indicated,  this  to 
be  maintained  by  monthly  prophylaxis,  at  least  until  the  case  is 
cured  and  then  continued  periodically  for  prevention. 

Antiseptic  mouth  washes  should  be  employed  frequently,  no 
matter  what  the  cause.  If  the  gum  tissue  be  soft  and  spongy, 
showing  signs  of  venous  hyperemia,  antiseptic  astringent  mouth 
washes  should  be  freely  used: 

I^ — Zinc,  chlorid gr-  x 

Aquge  menth.  pip fgj — M. 

Increase  as  desired. 

The  above  preparation,  used  in  spray  from  an  atomizer,  or,  if 
diluted,  as  a  wash  several  times  a  day,  is  an  excellent  local  application, 
meeting  both  indications.  Prescriptions  containing  eucalyptus  and 
benzoic  acid  are  excellent: 

I^ — Acid,  benzoic 3  parts 

Tinct.  eucalyptus 15  parts 

01.  menth.  pip 1  part 

Alcohol 100  parts 

Saccharin 2  parts — M. 

(Miller.) 

The  above  formula  diluted  one-half  is  agreeable  and  efficient. 
An  alkaline  1  per  cent,  salicylic  acid  wash  is  useful,  not  only  for 
the  gingivitis,  but  any  attendant  fetor  of  breath : 

I^ — Sodii  boratis 3iss 

Acidi  salicylici gr.  xv 

Aqua;  menthae  pip f  Siij — M. 


680     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 
The  following  is  astringent  and  antiseptic: 

I^ — Boroglycerini, 

Tinct.  krameriae, 
Tinct.  calendulge, 

Alcoholis aa      fgj^M. 

Sig. — One  or  two  teaspoonfuls  to  a  small  glass  of  water. 

Truman  advises  the  use  of  hydronaphthol  in  an  astringent  vehicle 
as  an  effective  germicide  for  use  by  a  patient : 

I^^Hydronaphthol gr.  x 

Glycerol fEJ 

Alcohol fSJ 

Aquse  destil fgj — M. 

Sig. — Use  as  a  wash  several  times  a  day.  (Pierce.l 

Talbot  recommends  for  gingivitis  the  following : 

I^ — Zinc  iodid 15  grams 

lodin 25  grams 

Glycerin 50  grams 

Water 10  grams— M.  - 

Sig. — Apply   to   gum    on   cotton  wound  on  an  applicator  and  dry  after  each 

painting.  (Talbot.^) 

The  following  is  a  5  per  cent,  formaldehyd  solution  which,  diluted, 
can  be  used  as  a  mouth  wash,  having  astringent  and  antiseptic 
qualities.  It  is  also  useful  in  various  strengths  as  a  germicide  for 
root  canals.     A  formula  for  quantity  is  given,  which  may  be  reduced 

in  prescriptions: 

No.  1 

I^— Thymol 5iss 

Menthol 3ss 

Oil  of  ecucalyptus, 
Oil  of  gaultheria, 
Oil  of  cassia, 

Oil  of  cloves aa    f  giss 

Alcohol fSiJ— M. 

No.  2 

Formaldehyd,  40  per  cent,  sol Oj 

Boric  acid, 

Sodium  biborate aa      giij 

Water Oij— M. 

No.  3 
Water  to gal.  j 

Make  up  No.  1  first  and  shake  well.  Place  No.  2  in  a  gallon 
demijohn  and  shake  well;  add  No.  1  and  shake  again;  add  No.  3 
and  shake  well.  For  dispensing  this  may  be  filtered;  for  ordinary 
use  this  is  not  necessary.  For  mouth  use  one-half  teaspoonf ul  is 
to  be  diluted  in  two  ounces  of  water,  making  a  1  to  600  formaldehyd 
solution. 

1  Dental  Cosmos,  1905,  p.  1312. 


MARGINAL  GINGIVITIS  681 

Equal  parts  of  Listerine  and  ordinary  distillate  of  hamamelis  is  a 
useful  combination.  Glycothymolin  is  a  very  popular  proprietary 
mouth  wash.  Lavoris  and  Vernas  lotions  are  agreeable  zinc  chloride 
washes  when  used  as  directed.  Phenol-sodique,  1  to  7  of  water 
is  quite  useful. 

For  mercurial  gingivitis  and  stomatitis  the  following  has  been 
rationally  recommended  •} 


I^ — Tinct.  myrrhjB fSiiJ 

Potassii  chloratis 3ss 

Sodii  chloridi 3ij 

Aquae  dis q.  s.  adfoviij — M. 

Sig. — Use  as  mouth  wash.     Repeat  every  two  hours. 

Fig,  611 


Showing  Vincent's  bacteria.      (Lederer.) 

All  mouth  washes  require  an  application  of  about  two  minutes' 
duration  at  least  twice  a  day  after  cleansing  the  teeth  in  order  to 
produce  the  best  effects.  As  this  is  somewhat  fatiguing  to  the  oral 
muscles,  several  applications  may  be  made,  one  after  the  other, 
until  the  total  is  attained  (Fig.  611). 

In  the  ulceration  gingivitis  due  to  Vincent's  bacteria  the  editor 
has  found  the  following  useful  as  a  germicidal  wash: 

I^ — Hydrargyri  bichloridi gr.  j 

Aquae  iiydrogenii  dioxidi fSiv — M. 

Sig. — Use  several  times  a  day. 

'  Medical  Press,  via  Dental  Cosmos. 


682     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

Vaughn^  recommends  silver  nitrate  15  to  30  grains,  water  fBj, 
Lugol's  solution,  chromic  acid  10  per  cent.,  zinc  chlorid  2  per  cent., 
and  argyrol  full  strength.  Lederer  uses  salvarsan  (see  p.  787) .  Curette- 
ment  is  sometimes  necessary.  Kirk^  recommends  in  addition  local 
application  of  tincture  of  iodin  and  irrigations  of  hot  water.  The 
glandular  enlargements  require  a  cold  compress  or  the  ice  bag. 

For  the  restoration  of  gum  tissue  between  molars  and  bicuspids 
L.  Ashley  Faughf^  has  recommended  applications  of  10  per  cent, 
trichloracetic  acid  on  an  orange-wood  stick  every  day  or  two  until 
the  case  is  cured. 


DEEPLY  SEATED  GINGIVITIS*  (INTERSTITIAL  GINGIVITIS, 

TALBOT). 

Definition. — This  may  be  defined  as  an  inflammation  characterized 
by  the  presence  in  the  deep  connective-tissue  elements  of  the  peri- 
cementum and  gum  tissue  of  an  excessive  number  of  leukocytes, 
attracted  thither  by  a  general  or  local  irritation  of  the  tissue  men- 
tioned. 

Local  Causes. — Any  of  the  local  causes  producing  marginal  gin- 
givitis, if  acting  deeply,  may  produce  a  deeply  seated  gingivitis.  In 
addition  to  these,  the  eruption  of  teeth,  the  wedging  of  them,  or 
their  movement  in  orthodontia,  the  overuse,  malocclusion,  or  dis- 
use, in  short,  any  of  the  causes  of  pericementitis,  septic  or  non- 
septic,  if  producing  inflammation  extending  beyond  the  confines  of 
the  pericementum,  are  causes  of  deeply  seated  gingivitis.  Pyorrhea 
alveolaris  is  a  suppurative  deeply  seated  gingivitis  and  pericemen- 
titis combined.  Ulceration  and  necrosis  following  extraction  cause 
gingivitis  (see  p.  633). 

If  at  any  time  pyogenic  infection  occur  at  the  gum  margin,  the 
purulent  phenomenon  of  pyorrhea  alveolaris  is  produced.  It  is  to 
be  understood  that  deeply  seated  gingivitis  presents  many  of  the 
features  of  pyorrhea  alveolaris  and  that  the  latter  is  a  gingivitis. 
The  conditions  are,  however,  pathologically  separable. 

The  following  is  a  good  example:  A  lady  presented  an  upper 
first  molar  which  had  had  a  pyorrhea  which  had  been  cured  by 
treatment  of  gum  margins  and  the  mesiobuccal  root  amputated. 
There  was  no  longer  any  appreciable  pus  pocket,  but  the  tooth 

1  Dental  Cosmos,  1912,  p.  655. 

2  American  Text  Book  of  Op.  Dent.,  p.  300.  '  Dental  Cosmos,  1905. 

4  The  writer  has  introduced  the  term  to  replace  interstitial  gingivitis,  not  to  multiply 
terms,  but  because  it  indicates  fairly  the  anatomical  situation.  Strictly  speaking, 
all  inflammations  are  interstitial. 


DEEPLY  SEATED  GINGIVITIS  683 

overoccluded  one-sixteenth  inch  and  had  tipped  forward.  It  was 
not  supported  mesially  or  distally  by  adjoining  teeth.  It  was  loos- 
ened. The  overocclusion  was  removed  by  grinding,  the  tooth  was 
wedged  against  its  mesial  neighbor,  and  a  distal  amalgam  filling 
contoured  out  to  its  distal  neighbor,  thus  affording  support  in  the 
direction  of  its  movement  in  mastication.  It  became  much  firmer. 
The  writer  considers  this  case  as  presented  for  diagnosis  one  of 
deeply  seated  gingivitis  due  to  malocclusion  and  non-support,  and 
not  a  case  of  pyorrhea.  In  like  manner  each  case  should  be  con- 
sidered on  its  own  symptoms. 

When  food  enters  the  interproximal  space  it  crushes  the  gum 
septum  and  later  depresses  it.  The  inflammation  causes  its  absorp- 
tion as  well  as  that  of  the  bone  septum,  so  as  to  leave  the  buccal  and 
lingual  portion  higher.  This  may  also  be  inflamed  and  further 
depressed.  The  pericementi  of  both  teeth  suffer  necrosis  to  the 
gum  level.  The  pocket  generally  finally  suppurates  and  a  lateral 
abscess  may  result  from  this  cause. 

While  this  may  be  classified  with  pyorrhea  alveolaris  it  seems  to 
the  writer  rather  a  distinct  form  of  deeply  seated  gingivitis,  at  least 
until  the  pus  flow  is  established.  The  writer  has  seen  another  form 
of  this  condition  in  which  caries  at  the  linguocervical  aspect  of  two 
molars  permitted  food  to  pack  laterally  (not  from  the  occlusal) 
under  tongue  pressure.  The  decay  proceeded  up  the  sides  of  the 
lingual  and  buccal  root  adjoining,  and  a  large  pocket  formed,  the 
gum  being  stripped  aw^ay.  The  wedging  out  of  the  gum,  touching 
with  silver  nitrate  after  cavity  preparation,  filling  with  amalgam, 
and  polishing  reduced  the  pocket  to  a  simple  one.  The  gum  grew 
in  as  far  as  it  could,  and  the  part  remains  relatively  healthy,  without 
pyorrhetic  symptoms,  but  food  collects  and  the  condition  may  become 
worse  again.  In  another  part  of  the  same  mouth  pus  was  found 
exuding  from  beneath  the  ulcerated  flap  of  gum  overlying  a  lower 
third  molar.  Otherwise  the  patient's  teeth  exhibited  no  pyorrhea. 
Such  cases  might  be  considered  pyorrhetic  if  pyorrhea  is  to  include 
ah  pus  flows  from  the  alveolus,  but  then  we  must  consider  apical 
abscess  such.  The  writer  believes  it  better  to  differentiate  the 
conditions. 

Systemic  Causes. — Systemic  causes  act  to  produce  a  deeply  seated 
gingivitis.  Drug  or  metal  poisoning,  or  auto-intoxication,  whether 
gastro-intestinal  or  by  leukomains,  and  acute  infectious  diseases, 
are  systemic  causes. 

A  case  of  spontaneous  loss  of  all  but  one  of  the  upper  teeth,  with 
subsequent  complete  alveolar  atrophy  as  the  result  of  the  trophic 
disturbance  from  peripheral  neuritis  in  a  tabetic  woman,  has  been 


684     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

reported  by  Gaucher  and  Dobrovici,  the  diagnosis  being  confirmed 
by  trophic  disturbance  in  the  foot  followed  by  plantar  perforation. 

It  seems  quite  certain  that  in  conditions  of  general  faulty  metab- 
olism substances  are  generated  in  the  s^^stem  or  are  retained  by 
reason  of  faulty  elimination,  and  which,  floating  about  in  the  blood 
stream,  act  as  irritants  to  the  pericementi  and  gum  margins  about 
the  teeth. 

Moreover,  the  pericemental  glands  seem  to  be  eliminating  organs 
which  may  become  overstimulated  and  thus  diseased. 

In  all  general  nutritional  disorders  parts  peripheral  to  the  circu- 
lation are  most  affected,  become  debilitated,  and  tend  to  a  degener- 
ative metamorphosis  of  cells. 

Rhein  found,  after  repeated  examinations  of  hospital  patients,  that 
"marginal  gingivitis  was  an  accompaniment  of  typhoid  fever,  tuber- 
culosis, malarial  disorders,  acute  rheumatism,  pleurisy,  pericarditis, 
and  syphilis,  among  the  acute  diseases.  Of  chronic  nutritional  dis- 
eases, it  was  commonly  observed  in  cases  of  gout,  diabetes,  chronic 
rheumatism,  several  forms  of  nephritis,  scurvy,  chlorosis,  anemia, 
leukemia,  and  pregnancy.  Also  in  disorders  of  the  central  nervous 
system  and  following  the  administration  of  mercury,  lead,  and  iodin." 

Rhein  states  that  the  gingivitis  produced  by  each  of  these  diseases 
has  distinctive  features  which  may  even  serve  as  diagnostic  signs  of 
the  nature  of  the  general  malady. 

Talbot's  experiments  in  the  mercurialization  of  dogs  (see  p.  644) 
demonstrate  that  efforts  upon  the  part  of  the  pericementum  to  elimi- 
nate the  bichlorid  of  mercury  result  in  a  non-septic  pericementitis, 
exhibiting  in  its  morbid  anatomy  the  characteristic  round-celled 
infiltration  of  inflammation. 

Black^  has  shown  that  a  gingivitis  produced  by  the  systemic 
administration  of  potassium  iodid  may  be  proved  to  be  caused  by 
its  elimination  by  the  pericemental  glands  by  test  of  the  gingival 
secretion  for  the  iodin  reaction. 

It  is  quite  reasonable  to  suppose  that  irritative  substances  origi- 
nating in  the  body  and  floating  in  the  blood  stream  may  act  in  like 
manner.     This  has  been  termed  auto-intoxication. 

Irritation  resulting  from  the  administration  of  mercury,  lead,  and 
iodin,  or  from  toxic  substances  absorbed  from  the  intestines,  is,  of 
course,  extrinsic  intoxication,  but  acts  in  the  same  manner. 

It  has  been  claimed  by  Hunter,  Herschell,  Goadby,  W.  B.  Keyes, 
D.  D.  Smith,  and  others,  that  the  toxins  formed  by  oral  fermenta- 
tions and  the  septic  infection  of  the  stomach,  intestines,  etc.,  arising 

'  American  System  of  Dentistry. 


DEEPLY  SEATED  GINGIVITIS  685 

from  the  mouth  are  competent  to  excite  a  train  of  systemic  dis- 
turbances ending  in  a  general  malnutrition. 

Certain  accomplished  cures  of  such  states  by  constant  oral  pro- 
phylaxis lend  plausibility  if  not  certain  proof  to  this  argument. 
Still,  the  malnutrition,  whatever  its  cause,  oral  or  otherwise,  may 
become  a  predisposition  by  lessening  the  resistance  of  the  soft  parts 
about  the  teeth  to  local  irritants  or  add  the  irritation  due  to  auto- 
intoxication. 

Talbot  claims  that  interstitial  gingivitis  is  largely  due  to  auto- 
intoxication due  to  intestinal  fermentation  with  production  of  by- 
products, notably  indol,  which,  when  absorbed,  may  or  may  not  be 
eliminated  through  the  eliminating  organs — liver,  kidneys,  skin,  and 
lungs — and  that  if  these  be  insufficient  to  the  task,  retention  occurs 
and  even  further  disease  of  the  organs  themselves,  especially  the 
kidneys.  Constipation  aggravates  the  condition,  if  not  producing 
it,  by  retention  of  fecal  matter  with  which  the  poisons  should  be 
eliminated.  The  overstrain  of  the  kidney  in  the  endeavor  to  take 
up  the  work  of  the  liver  (when  that  is  diseased)  in  elimination, 
produces  renal  inflammation  and  impairment  of  eliminative  func- 
tion. 

The  blood  is  surcharged  with  accumulated  poisons,  the  heart  and 
arteries  degenerate,  and  cardiac  hypertrophy  and  arteriosclerosis 
are  produced.  Blood  pressure  is  increased  and  end  artery  and  nerve 
degeneration  occur,  in  the  brain,  eye,  alveolar  process,  pulp,  etc., 
being  noticeable  first  in  the  gums.  He  draws  attention  to  the  transi- 
tory nature  of  the  alveolar  process  and  the  inability  of  the  arteries 
to  expand,  as  in  soft  tissues,  and  that  poisonous  products  settle  in 
the  end  arteries,  and  points  out  that  gingivitis  is  a  natural  result 
of  these  conditions.  The  demonstration  of  infarction  in  the  pulp 
due  to  systemic  conditions,  even  in  the  young,  has  been  made  by 
Hopewell -Smith,  and  also  indicates  end-artery  strain. 

Talbot  regards  indican,  the  absorbed  product  of  indol  in  the 
intestine  due  to  putrefaction  and  which  is  found  in  the  urine,  as  the 
excitant  of  gingivitis  in  intestinal  fermentation  (auto-intoxication) 
and  the  general  acidosis,  as  indicated  either  by  an  excess  of  acidity, 
in  the  urine  or  a  deficiency  therein,  as  excitant  in  various  conditions 
of  malnutrition. 

The  excess  of  acidity  above  40°  in  the  urine  indicates  excessively 
imperfect  oxidation,  while  defective  acidity  (below  30°)  indicates 
insufficiency  of  renal  elimination.  In  both  cases  systemic  acidosis  is 
the  condition.     (See  p.  103,  etc.) 

Diagnosis  of  Systemic  Causes. — The  diagnosis  of  systemic  cause 
bv  malnutritional  conditions  involves  almost  the  entire  range  of 


686     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

medical  diagnosis,  a  subject  obviously  beyond  the  scope  of  this 
work.  If  local  causes  do  not  explain  the  oral  pathological  condi- 
tion it  is  well  to  refer  the  patient  to  a  competent  medical  diagnos- 
tician for  examination  and  treatment.  Urinalysis  or  salivary  analysis 
may,  however,  be  made  by  either  the  dentist  or  a  specialist  in  that 
work,  and  together  with  symptoms  some  information  may  be  gained. 
Talbot  directs  that  twenty-four-hour  urine  should  be  obatined  and 
the  following  points  looked  for.^ 

Amount. — This  should  be  about  forty  ounces. 

Specific  Gravity. — If  high,  it  indicates  an  increased  proportion  of 
solids  per  ounce. 

Degree  of  Acidity. — If  above  40°  it  indicates  acidosis  by  imperfect 
oxidation;  if  below  30°  it  indicates  renal  insufficiency  and  retention 
in  blood  of  acid  products. 

Indican. — If  present,  it  always  indicates  intestinal  fermentation. 

Albumin. — Not  of  certain  origin. 

Hyalin  Casts. — If  bloody,  they  indicate  renal  inflammation. 

Compound  Hyalin  and  Coarsely  Granular  Casts  and  Waxy  and  Amyloid 
Casts. — Indicate  changes  in  structure  of  kidney. 

Symptoms. — Headache,  loss  of  appetite,  loss  of  memory,  irrita- 
bility, biliousness,  fatigue,  muscle  soreness,  hypochondriasis,  in- 
somnia, vertigo,  muddy  complexion,  tinnitus  aurium,  general  ner- 
vousness, cold  extremities,  impotence,  leg  cramps,  twitching  of 
muscles,  neurasthenia,  pruritus,  acne,  urticaria,  arteriosclerosis,  gout, 
rheumatism,  Bright's  disease,  diabetes,  uric  acid  diathesis,  nervous 
disorders,  asthma,  anemia,  lethargy,  stupor,  insanity,  etc.,  are 
symptoms  which,  in  part,  may  develop  from  the  auto-intoxication 
by  the  toxins  and  acidosis.     (See  General  Malnutrition.) 

Unnatural  odor  of  the  breath,  armpits,  and  thighs  indicate  an 
effort  of  the  lungs  and  skin  at  elimination.^ 

Lead  poisoning  occurs  in  those  using  white  lead,  as  painters.  The 
occupation  together  with  paralysis  of  the  extensors  as  in  wrist  or 
foot-drop,  tremors,  and  peripheral  anaesthesia  from  toxic  peripheral 
neuritis  and  the  blue  lead  line  upon  the  gum  are  diagnostic  points 
with  which  mercurial  symptoms  of  like  character  may  be  confused 
through  urinalysis  for  lead;  the  history  and  occupation  clear  it  up. 

In  mercurial  poisoning  the  occupation,  history  of  drug  adminis- 
tration, salivation,  enlarged  tongue,  general  pericementitis  or  gingi- 
vitis, urinalysis  for  mercury,  will  clear  the  diagnosis  as  against 
that  of  lead  poisoning. 

1  Interstitial  Gingivitis  due  to  Auto-intoxication,  Journal  American  Medical  Asso- 
ciation and  Dental  Digest,  1906. 

2  Talbot. 


DEEPLY  SEATED  GINGIVITIS 


687 


Pathology  and  Morbid  Anatomy. — The  local  or  systemic  causes 
produce  direct  inflammation;  the  bloodvessels  become  overful,  and 
waste  products  collected  in  the  end  arteries  produce  local  degenera- 
tion, diapedesis  of  leukocytes  into  the  interstitial  submucous  gum 
tissue  occurs,  and  the  spaces  are  filled  with  inflammatory  exudate. 
The  papillae  become  enlarged  and  the  epithelial  layer  undergoes  an 
increase  in  formation  of  cells  (hyperplasia).  The  gum  in  consequence 
of  these  changes  becomes  swollen,  its  color  deepened,  and  it  bleeds 
readily. 


Fig.  612 


Fig.  613 


Fig.  614 


Resorption  of  alveolar  process  due  to  interstitial  gingivitis,  caused  by  marginal  irri- 
tation from  excessive  filling  material.     (Radiographs  by  Price.) 


If  the  process  be  advanced  the  alveolar  process  is  involved. 

After  a  time  the  effects  of  continued  low-grade  inflammation  are 
expressed  in  resorption  of  bone  or  cementum,  or  both,  or  hyper- 
trophy of  bone  or  cementum,  or  both,  as  the  two  processes  may  be 
in  evidence  at  the  same  time. 

Talbot  describes  several  forms  of  bone  resorption  occurring  in 
interstitial  gingivitis : 

(a)  Lacunar  resorption  carried  on  by  the  osteoclasts  normally 
lying  upon  the  surface  of  the  bone.  Under  irritation  they  increase 
in  number  and  excavate  irregular  bays  in  the  bone  (Howship's 
lacunae).  These  are  then  deepened  and  widened,  destroying  areas 
of  bone.     (See  p.  146.) 

(6)  Perforating  canal  resorption  beginning  in  the  small  canals 
normally  perforating  the  trabecule  of  bone  in  various  directions  and 
transmitting  the  bloodvessels  from  one  medullary  space  or  Haver- 
sian canal  to  another  (Volkmann's  canals).  The  osteoclasts  widen 
these,  necessarily  reducing  the  substance  of  the  trabeculse  (Fig.  71). 

(c)  Halisteresis  ossium,  beginning  with  a  decalcification  of  masses 
of  the  bone,  the  organic  matrix  being  for  a  time  undisturbed,  but  is 
later  removed.  This  is  a  local  expression  of  what  may  occur  in  other 
bones  of  the  body  in  the  condition  known  as  osteomalacia  (Fig.  74). 

According  to  Talbot,  premature  resorption  of  the  alveolar  margins, 


688     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

either  local  or  general,  is  due  to  this  process,  called  by  him  alveolar 
osteomalacia,  and  occurs  in  pregnancy  or  senility,  as  a  rule. 

He  states  that  the  decalcified  bone  may  be  recalcified  after  con- 
finement in  pregnancy,  but  is  never  restored  in  senility. 

A  lesser  degree  of  irritation  may  set  the  osteoblasts  at  work  and 
cause  the  building  up  of  the  alveolar  process,  either  as  a  restoration 
of  resorbed  bone  or  as  an  hypertrophy  of  either  the  alveolar  process 
or  the  cementum  of  the  root  (hypercementosis) . 

Endarteritis  obliterans  is  a  thickening  of  the  intima  of  an  artery 
or  capillary,  due  to  chronic  irritation,  and  causing  a  lessening  of  the 
lumen  of  the  vessel,  even  to  the  point  of  obliteration  of  the  capillaries. 

The  blood  flow  is  impeded  and  nutrition  of  cells  impaired.  Any 
cause  of  deeply  seated  inflammation  may  produce  it.  In  all  cases 
of  chronic  deeply  seated  gingivitis  the  bloodvessels  are  so  diseased 
(Figs.  615  and  616). 

Fig.  615  Fig.  616 


Fig.  615. — Longitudinal  section  of  gingival  border,  showing  round-cell  inflamma- 
tion, due  to  mercury,  and  extending  to  the  inner  coat  of  the  bloodvessel,  and  also 
plasma  mast  cells.    From  a  dog.    (Talbot.) 

Fig.  616. — Endarteritis  obliterans :  A,  adventitia;  £■,  elastic  tissue  between  middle 
coat  and  intima;  M,  muscular  coat;    J,  thickened  intima.     (Talbot,  after  Kaufmann.) 

Local  Treatment. — The  treatment  must  be  directed  to  the  removal 
of  the  underlying  cause.  All  local  causes  must  be  removed  and  the 
teeth  put  into  physiological  use  as  far  as  possible.  This  includes 
the  removal  of  causes  of  malocclusion  or  overuse;  of  the  crowding  of 
food  between  teeth,  the  removal  of  local  mechanical  irritants  and 
infective  agents.     The  local  treatment  in  general  is  that  employed 


DEEPLY  SEATED  GINGIVITIS  689 

for  marginal  gingivitis  or  for  pyorrhea  alveolaris.  (See  p.  677;  also 
Pyorrhea  Alveolaris.) 

Systemic  Treatment. — This,  of  course,  depends  upon  the  systemic 
condition  and  its  causes,  but  if  due  to  torpid  biliary  function  or 
defective  elimination  with  consequent  retention  of  body  products, 
the  restoration  of  the  eliminative  function  should  be  aimed  at.  In 
intestinal  auto-intoxication  impacted  fecal  matter  should  be  removed 
by  repeated  injections,  if  necessary,  of  warm  water,  and  the  bowels 
be  kept  clear  by  flushing  with  soap  and  water  once  or  twice  a  week. 
The  massage  of  the  abdomen  restores  the  tonicity  of  the  bowels. 
The  bile  function  should  be  restored,  and  the  bile  be  increased  in 
flow  by  calomel  and  soda,  yV  to  ^  gr.,  every  hour  until  1  grain  is 
taken;  to  be  followed  by  a  saline  laxative  (as  Seidlitz  powder);  or 
podophyllin,  yV  to  I  gr.,  up  to  |  gr.,  may  be  given  instead  of  calomel. 

Talbot^  also  uses* 

I^ — Aloin J  gr. 

Strychnin  sulphate eV  S^"- 

Extract  of  belladonna .      .      .      .      |^  gr. 

Pulv.  ipecac xV  gr. — M. 

Take  at  bedtime  and  follow  with  a  saline  cathartic  next  morning. 
If  the  stools  remain  unhealthy,  administer  each  two  to  four  hours  2 
to  5  grs.  of  compound  lime,  soda  and  zinc  carbolate  until  the  stools 
are  healthy. 

To  continue  the  stimulation  of  the  liver  administer  bilin  tV  to 
J  gr.  four  or  five  times  a  day. 

The  urine  should  be  examined  for  evidence  of  established  disease, 
and  if  this  be  found  the  patient  referred  to  a  general  practitioner. 
(See  General  Malnutrition.)  If  found  only  symptomatic  of  hepatic 
or  renal  insufficiency  and  nutritional  disorder,  the  amount  of  urine 
should  be  increased  to  40  ounces  by  the  drinking  of  3  pints  of  water 
(including  table  beverages)  per  day,  which  will  aid  bowel  and  renal 
elimination  and  flush  tissues  of  accumulations,  including  retained 
acids.  If  the  urine  be  abnormally  acid  (above  40°)  administer 
3-gr.  tablet  of  lithia,  sodium  bicarbonate,  or  sodium  chlorid  in  a  glass 
of  water  four  times  a  day.  Hot  or  Turkish  baths  keep  the  skin 
free  for  eliminative  function.  Well-apportioned  rest  and  exercise 
and  moderate  eating  of  proper  nutritious  food  are  indicated.  (See 
pp.  97  and  105.)  When  organic  disease  is  present  the  treatment 
should  be  relegated  to  the  medical  practitioner. 

1  Therapeutics  and  Treatment  of  Intestitial  Gingivitis,  Dental  Digest,  1906. 
44 


690     PERICEMENTAL  DISEASES  BEGINNING  AT  GUM  MARGIN 

MARGINAL  ATROPHY  OF  THE  GUMS. 

In  advanced  age  there  exists  often  a  tendency  of  the  gums  to 
shrink  evenly  away  from  the  enamel,  exposing  the  cementum.  Hope- 
well-Smith describes  this  as  accompanied  by  fibroid  degeneration 
of  the  pericementum  (which  see),  and  regards  the  latter  as  a  purely 
senile  change. 

It  may  be  noted  upon  the  buccal  side  only  of  a  denture,  and  be 
due  to  vigorous  brushing. 

It  is  also  seen  localized  at  cervices  next  to  a  space  from  which  a 

tooth  has  been  extracted.     In  one  case  the  editor  saw  a  slightly 

hypertrophied  gum  distinctly  overlapping  a  cavity  margin  drawn 

back  one-eighth  inch  within  a  month  as  the  result  of  extraction  of  the 

adjoining  root. 

Fig.  617 


Recession  of  gum  in  senility;   beginning  decalcification  of  cementum;   alveolar  resorp- 
tion  after  extraction.     (Philadelphia  Dental  College  Museum.) 

Apart  from  senile  changes,  and  possibly  even  including  them, 
these  effects  seem  to  be  the  result  of  an  overstimulation  of  the  gums 
resulting  in  atrophy.  It  may  be  that  collections  upon  the  teeth 
are  in  some  degree  responsible.  The  gums  have,  for  the  most  part, 
a  healthy  look,  but  are  in  a  condition  predisposed  to  pyorrhea 
alveolaris. 

Treatment. — If  localized  and  the  restoration  of  the  gum  be  desir- 
able,  Harlan's  method  may  be  tried. ^     (1)   Cleanse  the  exposed 

1  Dental  Cosmos,  1906,  p.  927,  and  1907,  p.  598, 


MARGINAL  ATROPHY  OF  THE  GUMS  691 

tooth  surface  and  slightly  roughen  it  near  the  gum  margin.  (2) 
Dissect  away  the  gum  from  the  root  to  about  one-quarter  inch  in 
depth,  wiping  the  blood  away  carefully  with  mouth  open  until 
hemorrhage  ceases  spontaneously,  or  check  with  adrenalin  solution. 
(3)  Make  three  incisions  into  and  through  the  gum  tissue.  (4) 
When  bleeding  has  almost  ceased  fill  the  cuts  with  dried  zinc  iodid, 
allowing  the  blood  to  liquefy  it  so  that  it  may  be  carried  around 
the  gum  margin.  This  creates  a  profound  irritation,  which  should 
not  be  disturbed.  (5)  The  patient  should  use  a  mild  antacid  anti- 
septic wash,  as  of  sodium  bicarbonate  or  milk  of  magnesia.  (6)  Re- 
peat three  or  four  times  at  intervals  of  three  or  four  weeks,  with 
cuts  in  a  new  location.  (7)  Use  silk  or  pure  silver  ligatures  around 
the  teeth  under  the  gum  for  further  irritation.  (8)  To  allay  over- 
irritation  paint  with  1  part  adrenalin  and  3  parts  compound  tincture 
of  iodin  once  in  three  days. 

Harlan  states  that  a  long  time  may  be  required  in  some  cases.  It 
should  not  be  attempted  over  a  gold  filling,  but  an  unglazed  porcelain 
may  be  covered,  though  no  attachment  will  exist.  The  principle 
involved  is  that  of  coaxing  the  gum  into  adherence  with  the  roughened 
root,  and  the  filling  in  of  the  cut  with  scar  tissue. 

As  a  wash  use: 

IJ — Hydronaphthol gr.  xx 

Oil  eucalyptus lUx 

Oil  cassia lUx 

Alcohol fSiiJ 

Distilled  water foxiij — M. 

Sig. — Use  freely  five  or  six  times  daily,  diluted,  if  necessary,  with  more  water. 

The  gums  should  not  be  brushed  for  several  days  after  operating. 
Avoid  insoluble  dentifrices.  If  this  treatment  be  considered  inad- 
visable the  appearance  in  a  given  case  may  be  improved  by  the 
use  of  a  pink  porcelain  inlay. 

For  general  recession  due  to  osteomalacia  the  general  acidosis 
may  be  treated. 


CHAPTER  XXIII. 
SALIVARY  AND  SERUMAL  CALCULUS. 

Calculi  are  more  or  less  hard  concretions  found  in  varying  situa- 
tions and  composed  of  inorganic  and  organic  matter  combined  in  an 
unknown  manner. 

As  related  to  the  teeth,  calculi  arise  from  the  following  recognized 
sources : 

1.  Obviously  from  the  saliva,  and  deposited  in  situations  which 
clearly  indicate  its  source,  salivary  calculus  (or  ptyalogenic  calculus 
— Peirce) . 

2.  From  the  serum  of  the  blood  deposited  at  some  point  along  the 
side  of  the  root  between  the  gum  margin  and  the  apex  of  the  root, 
and  called  serumal  calculus  (Black),  or  sanguinary  calculus  (Inger- 
soll).     Of  this  there  are  several  varieties: 

(a)  That  associated  with  a  probable  fermentation  and  an  altered 
secretion  from  the  gum  margin,  and  known  as  subgingival  calculus. 

(6)  That  occurring  in  situations  in  which  a  chronic  pus  flow  is 
found,  whether  apical  or  subgingival,  and  which  may  be  called 
pyogenic  calculus. 

(c)  That  found  upon  the  roots  of  teeth  at  a  point  to  which  saliva 
has  no  access  and  over  which  pus  does  not  flow,  and  which  is  there- 
fore deposited  by  the  lymph  derived  from  the  blood,  and  to  which 
the  appellation  hematogenic  calculus  (Peirce)  is  applicable. 

In  this  class  Kirk  found  two  varieties  resulting  from  pericemental 
inflammation:  (1)  Subpericemental  deposits,  and  (2)  intraperice- 
mental  deposits.^ 

These  several  names  will  be  adhered  to  in  further  descriptions  as 
having  definite  significance. 

SALIVARY  CALCULUS. 

Definition. — Salivary  or  ptyalogenic  calculi  are  hard  formations 
composed  of  salts  of  the  saliva  which  have  been  deposited  or  precipi- 
tated and  combined  in  an  unknown  manner  with  organic  substances, 
probably  mucin  or  globulin. 

1  Dental  Cosmos,  1905. 
(692) 


SALIVARY  CALCULUS 


693 


Occurrence. — They  are  found  upon  the  surfaces  of  the  teeth, 
notably  in  situations  opposite  the  mouths  of  the  saHvary  glands,  in 
the  ducts  of  the  muciparous  salivary  glands  (sublingual  and  sub- 
maxillary), and  upon  artificial  dentures.  A  photograph  of  a  plate 
containing  an  enormous  mass  of  calculus,  the  result  of  seven  years' 
accumulation,  is  shown  in  Fig.  618.  The  teeth  are  occasionally 
buried  in  it.  The  editor  extracted  three  lower  incisors  whi-ch  had 
been  wired  together,  and  were  absolutely  covered  from  the  neck  to 
the  apex  by  calculus. 

Varieties. — Clinically  two  distinct  varieties  of  salivary  calculus  are 
recognizable:  (1)  The  soft,  friable,  whitish  yellow  deposits  found 
chiefly  upon  the  buccal  surfaces 

of  the   upper  molars   and  upon  ^^^-  ^is 

the  lingual  surfaces  of  the  lower 
anterior  teeth;  (2)  dark-colored 
and  hard  deposits  found  more 
frequently  in  the  latter  situation, 
less  frequently  in  the  former. 

Origin  of  Salivary  Calculus. — 
The  origin  of  salivary  calculus 
may  be  studied  from  several 
standpoints:  (1)  The  formation 
of  calculi  in  other  parts  of  the 
body;  (2)  an  analysis  of  saliva 
and  salivary  calculi;  (3)  extra- 
oral  experiments  upon  saliva 
with  a  view  to  the  formation 
of  salivary  calculus  extra-orally; 

(4)  the  changes  observed  clinically  in  salivary  calculus  during  its 
deposition. 

Ziegler^  states  that  all  free  concretions  have  an  organic  basis  or 
nucleus  (inspissated  feces,  vegetable  material,  epithelial  scales, 
mucus,  etc.). 

As  to  cholesterin  gallstones,  he  states  that  if  the  cholesterin  be 
dissolved  out  by  ether,  a  yellowish  organic  matrix  remains  which 
retains  the  form  of  the  stone  and  presents  upon  examination  radiating 
spaces  formerly  occupied  by  the  crystals.  He  describes  the  forma- 
tion of  the  gallstone  as  an  infiltration  or  incrustation  of  degenerated 
organic  matter  (epithelial  scales,  etc.)  with  cholesterin,  bile  pigment, 
etc.,  to  which,  after  a  nucleus  is  formed,  other  portions  are  added  in 
like  manner. 


Salivary  calculus  attached  to  a  lower 
partial  plate  worn  seven  years  without 
removal.  Shows  form  of  sublingual 
space.  Practice  of  Dr.  Ford,  Toulouse, 
France.  (Specimen  in  possession  of 
Philadelphia  Academy  of  Stomatology.) 


1  General  Pathology. 


694  SALIVARY  AND  SERUMAL  CALCULUS 

Of  urinary  calculi  he  states  that  Ebstein  has  shown  an  organic 
substance  albuminous  in  nature  to  be  left  after  dissolving  out  the 
various  salts. 

In  stratified  calculi  this  stroma  also  shows  stratification.  Such  a 
stroma  may  be  seen  after  decalcification  of  a  bit  of  salivary  calculus. 

Analysis  of  salivary  calculus  shows  it  to  be  composed  of  about  22 
per  cent,  of  water  and  organic  matter  as  the  portion  removable  by 
burning  the  calculus,  and  about  78  per  cent,  inorganic  matter  as  the 
portion  removable  by  decalcification  with  acids. 

Following  are  the  analyses  of  salivary  calculus  by  Stevenson  and 
Schehevetskey,  respectively  •} 

Soft  tartar  Hard  tartar  on 

on  molars.  lower  incisors. 

Water  and  organic  matter 21.48  17.51 

Magnesium  phosphate 1.31  1.31 

Calcium  phosphate  with  a  little  carbonate  and 

trace  of  fluorid 77 .  21  81 .  18 

100.00  100.00     . 

Water  and  organic  matter 22 .  07 

Magnesium  phosphate         1.07 

Calcium  phosphate 67.18 

Calcium  carbonate 8 .  13 

Calcium  fluorid 1 .  55 

100.00 

These  observers  are  practically  agreed  upon  the  substances  present 
in  calculus  as  mainly  calcium  phosphate  with  some  calcium  carbonate, 
calcium  fluorid,  and  magnesium  phosphate  combined  with  organic 
matter. 

Talbot  furnishes  the  following  analysis  of  serumal  calculus  by 
J.  H.  Salisbury :2 

Water  and  organic  matter        .      .      . 32 .  24 

Magnesium  phosphate  . 0.98 

Calcium  phosphate 63 .  08 

Calcium  carbonate 3.70 

100.00 

To  these  Kirk^  adds  ammoniomagnesium  phosphate  as  a  product 
of  putrefaction. 

According  to  Mitscherlich,^  parotid  saliva  contains  globulin,  but 
no  mucin,  and  contains  calcium  carbonate;  calcium  phosphate  being 
present  in  but  minute  amount.  The  submaxillary  saliva  contains  a 
large  amount  of  mucin,  which  gives  to  mixed  saliva  its  viscid  nature. 

1  Talbot.    Interstitial  Gingivitis.  ^  Ibid. 

3  Dental  Cosmos,  1905,  p.  752. 

^  Halliburton.    Physiological  and  Pathological  Chemistry. 


SALIVARY  CALCULUS  695 

Analyses  of  submaxillary  saliva  and  mixed  saliva  by  Bidder  and 
Schmidt  gave  the  following  results: 

Submaxillary  Saliva.    ' 

Water 991.45 

Organic  matter 2 .  89 

Calcium  chlorid 

Sodium  chlorid 

Inorganic  matter    < 


4.50 


Calcium  carbonate 

Calcium  phosphate  j- 1 .  16 

Magnesium  phosphate 

1000.00 

Mixed  Saliva, 

Water 995.16 

Epithelium 1.62 

Soluble  organic  matter 1 .  .34 


Organic  matter  . 


Potassium  sulphocyanid 0.06 

Inorganic  matter   \   Sodium,  calcium,  and  magnesium  phosphate     0.98 
Sodium  and  potassium  chlorid      .      .      .  0.84 


1000.00 


That  an  error  of  experiment  or  estimation  exists  in  these  analyses 
is  shown  by  the  fact  that  calcium  carbonate  is  not  mentioned  as 
existing  in  mixed  saliva,  while  it  exists  in  submaxillary  saliva;  this 
is  a  physical  impossibility. 

It  is  presumptive,  however.,  that  calcium  carbonate  has  not  been 
specially  estimated. 

If  a  bit  of  calculus  be  dried  and  then  burned  at  a  red  heat,  the 
organic  matter  present  will  burn  out,  the  calculus  retaining  its  form. 
If  a  similar  bit  be  subjected  to  dilute  acid  (1  per  cent,  nitric)  the 
inorganic  matter  will  be  removed,  the  calculus  will  float  to  the  top 
of  the  liquid,  and,  after  a  time,  remain  as  a  light  stroma  of  nearly 
the  original  form  of  the  piece. 

If  a  bit  of  calculus  be  transversely  ground,  it  is  seen  under  a  low- 
power  lens  to  present  a  laminated  appearance — i.  e.,  it  has  been 
deposited  in  layers  representing  periods  of  activity.  The  under 
surface  of  the  calculus  shows  a  concentric  formation.  Beneath  the 
mass  a  nidus  of  darker  calculus  may  be  found,  and  if  section  of 
extensive  calculi  be  made  the  greenish  deposits  may  be  seen  scattered 
through  the  mass.  Black  has  noted  the  presence  of  urates  in  nearly 
all  specimens  examined  by  the  murexid  test.  Foreign  bodies  are 
sometimes  entangled  in  the  mass.  Peirce  recorded  a  case  in  which 
a  small  clasp  plate  was  securely  fastened  to  the  teeth,  and  the  patient 
denied  possession  of  such  a  substitute. 

In  some  cases  extensive  salivary  deposits  are  found  associated 
with  highly  offensive  odors — i.  e.,  putrefaction  of  the  organic  matter 


696  SALIVARY  AND  SERUMAL  CALCULUS 

occurs  as  a  part  of  the  process — indeed,  bacteria  are  constantly 
associated  with  the  mass  and  may  furnish  their  quota  of  the  organic 
matter.  Extraneous  matters,  such  as  tobacco  smoke  or  other  pig- 
ments, cause  discoloration  of  the  mass.  With  data  relative  to  the 
physical  and  chemical  analysis  of  calculi,  the  mode  of  calculus  forma- 
tion may  be  studied.  It  will  be  noted  that  the  necessary  elements 
of  calculus  formation  are  supplied  by  the  saliva  and  food  debris — 
i.  e.,  an  organic  basis  is  furnished  in  which  calcium  salts  may  be 
entangled,  precipitated,  or  chemically  combined. 

If  a  test-tube  be  filled  with  saliva  and  allowed  to  remain  at  rest 
for  several  days,  a  flocculent,  light  yellow  precipitate  will  be  noted 
at  the  bottom  of  the  tube.  If  the  supernatant  fluid  be  drawn  off 
with  a  pipette  and  the  precipitate  be  allowed  to  dry,  it  will  be  found 
possessed  of  the  chief  characteristics  of  calculus — hardness,  friability, 
a  light  yellow  color,  tenacity  of  adherence  to  objects  with  which  it 

is  in  contact,  and  capability  of 
analysis  into  organic  matter  and 
inorganic  salts. 

The  blood  contains  about  0.8 
per  cent,  of  inorganic  salts,  includ- 
ing those  found  in  salivary  calculi, 
and  a  certain  percentage  of  them 
is  also  found  in  the  blood  cor- 
puscles.    The}^  probably,  there- 
fore, exist  in  body  cells  in   some 
proportion. 
The  salts  are  also  taken  into  the  body  in  the  form  of  food.     Their 
appearance  in  the  various  excretions  and  secretions  of  the  body  is  to 
be  regarded  as  in  all  probability  an  effort  upon  the  part  of  the  system 
to  eliminate  a  superabundance  of  inorganic  material  from  the  body. 
The  ingestion  of  quantities  of  animal  or  vegetable  food  rich  in 
phosphates,  or  the  excessive  liberation  of  the  phosphoric  acid  in 
malnutrition,   may  produce   an   excessive   elimination   of   these   in 
the  excretions  and  cause  a  tendency  to  the  production  of  calculi 
about  the  body.    This  condition,  known  as  phosphaturia,  is  observed 
in  certain  nervous  diseases,  rachitis,  osteomalacia,  leukemia,  gout, 
and  rheumatism,^  in  which  the  phosphaturia  is  symptomatic  of  an 
excessive   katabolism;    also   in   intestinal   disturbance   resulting   in 
imperfect  assimilation  of  food.     (See  p.  111.) 

Whether  taken  in  as  food  or  liberated  during  metabolism  it  is 
probable,  as  pointed  out  by  Talbot,  that  if  one  excretory  organ  fail 

1  Thompson.    Practical  Medicine. 


SALIVARY  CALCULUS  697 

to  perform  its  office  in  full  degree  another  must  take  up  its  work. 
For  this  reason,  in  any  bodily  condition  aifecting  elimination  a 
superabundance  of  inorganic  salts  may  appear  in  the  blood  and 
hence  in  the  saliva,  and,  probably,  in  even  the  secretions  from  the 
gingival  margins. 

That  the  deposit  of  calculus  may  have  some  dependence  upon  the 
superabundance  of  calcium  salts  in  the  saliva  is  evidenced  by  the 
fact  that  in  young  children  but  little  calculus  is  deposited  upon 
the  teeth,  though  the  oral  fermentation  is  not  lacking.  The  salts 
are  needed  in  bone  formation. 

The  Organic  Factor  of  Calculus  Formation. — Black^  has  argued 
from  experiment  that  the  organic  basis  is  probably  a  colloidal  agglu- 
tinating substance  precipitated  from  saliva  in  the  form  of  small 
oval  or  cylindrical  globules,  made  up  of  a  mulberry  mass  of  fine 
globules.  This  substance  he  has  called  "agglutinin."  This  lodges 
upon  solid  objects  and  the  minute  particles  of  inorganic  salts  are 
precipitated  into  this. 

This  substance  is  coagulated  (white)  at  200°  F.,  but  as  freshly 
deposited  is  transparent,  and  has  a  soft,  greasy,  sticky  feel.  Micro- 
organisms multiply  in  it  after  a  time,  but  at  first  it  is  free  from 
them.  Black  has  shown  that  this  deposit  precedes  the  infiltration 
by  the  salts. 

Black  regards  this  substance  as  some  product  of  faulty  metab- 
olism, and  as  the  determining  factor  in  calculus  formation  rather 
than  the  presence  of  more  or  less  calcium  salts,  and  believes  this  to 
account  for  fluctuation  in  deposit.  He  found  that  the  use  once  of 
Epsom  salt  as  a  cathartic  w^ould  stop  the  accumulation  of  calculus 
for  from  a  few  days  to  several  weeks,  according  to  the  condition  of 
the  patient.  He  regards  the  condition  as  not  due  to  constipation, 
but  rather  due  to  the  formation  of  a  larger  quantity  of  chyle  than 
can  be  readily  assimilated.  In  his  own  case  he  was  able  to  limit 
calculus  formation  by  reducing  the  intake  of  food  and  thorough 
mastication,  and  to  bring  it  on  at  will  by  partaking  heartily  of  rich 
foods."     The  subject  requires  further  investigation. 

Exposure  of  the  roots  of  teeth,  especially  the  lower  anterior  ones, 
favors  the  deposition  of  calculus,  owing  to  the  difficulty  of  brushing 
the  surfaces. 

^  Items  of  Interest,  June,  1911. 

-  It  is  known  that  about  one-third  of  calcium  and  other  salts  are  eliminated  in  the 
intestinal  secretion.  It  is  therefore  not  certain  from  Black's  experiments  ■udth  Epsom 
salt  whether  the  salts  necessary  for  calculus  formation  are  not  so  eliminated  because 
of  the  stimulation  of  secretion  from  the  surface  of  the  swept  and  stimulated  intestine. 
The  fact  that  the  quality  of  the  chyle  remained  the  same  during  the  several  weeks  of 
lessened  calculus  formation  seems  rather  to  prove  that  retention  of  some  organic 
or  inorganic  factor  is  of  more  importance  than  the  quantitj^  of  chjde  formed.  Again, 
a  lessened  ration  may  reduce  the  quantity  of  the  factors. 


698 


SALIVARY  AND  SERUMAL  CALCULUS 


That  rest  or  relative  quiescence  of  the  saliva  is  favorable  for  the 
formation  of  calculus  is  shown  by  the  fact  that  it  occurs  at  points 
which  are  ordinarily  not  subjected  to  agitation — i.  e.,  buccal  surfaces 
of  upper  molars,  lingual  and  labial  surfaces  of  lower  incisors. 

Adhesive  precipitations  of  newly  formed  and  very  soft  calculus 
form  in  these  latter  situations  in  the  course  of  twenty-four  hours. 
If  not  removed  by  brushing  they  harden  and  thicken.  An  unused 
side  of  a  denture  often  accumulates  calculus  in  greater  degree  than 
the  side  used  for  mastication.  This  does  not  occur,  however,  if  the 
brush  be  used  properly  and  equally  vigorously  upon  both  sides. 


Fig.  620 


Fig.  621 


Unclean  necks  of  teeth,  salivary  calculus, 
and  green  stain.  (Philadelphia  Dental  Col- 
lege Museum.) 


A,  maxillary  sinus;  jB,  duct  of  Steno ; 
C,  parotid  calculus;  E,  submaxillary 
gland.  ^ 


Burchard  pointed  out  that  irritations  of  various  natures  about 
the  teeth  and  gums  may  by  reflex  action  cause  secretions  of  fluid, 
abnormal  in  quantity  and  quality,  from  both  the  salivary  glands  and 
the  buccal  parietes  (glands  and  gum  margins) .  It  is  more  probable, 
however,  that  the  systemic  condition  and  uncleanliness,  together 
with  tooth  form,  is  largely  responsible.  The  editor  has  a  patient 
who  is  abstemious,  eats  moderately,  exercises  indefatigably  in  the 
open  air,  and  drinks  water  freely.  During  the  golf  season,  when 
perspiration   is   free,  he   has   somewhat   less   calculus,   but   always 


SALIVARY  CALCULUS 


699 


has  some  at  uncleansed  spots.     This  appears  within  two  weeks  of 
prophylaxis. 

An  increase  of  oral  fermentation  is  commonly  associated  with  an 
excess  of  calculus  formation,  but  conditions  of  oral  fermentation 
may  be  seen  in  which  but  little  deposit  occurs.  The  mouths  of 
many  children  are  examples  of  this. 


C,  calculus;   S.L.C.,  sublingual  cavity;   S.L.GL.,  sublingual  gland. 
Fig.  623 


Right  side,  abrasion  from  overuse;   left  side,  deposits  due  to  stagnation. 


Calculi  harden  with  age.  It  is  commonly  noted  that  soft  calculus 
may  be  readily  removed  with  a  brush.  Calculus  deposited  upon 
lower  teeth  within  a  week  or  two  after  a  thorough  cleansing  may  be 
scraped  away  as  a  cheesy  mass;  after  a  much  longer  time  it  comes 


700 


SALIVARY  AND  SERUMAL  CALCULUS 


away  as  a  hard  scale.  In  very  old  deposits  it  may  be  exceedingly 
hard  and  quite  firmly  attached  to  the  teeth. 

These  clinical  observations  confirm  the  deduction  that  an  infiltra- 
tion of  calcium  salts  occurs  in  the  organic  stroma  of  the  calculus, 
analogous  to  that  occurring  in  dead  or  degenerative  tissue  throughout 
the  body  (calcareous  infiltration  or  degeneration).  It  is  probable 
that  a  firmer  chemical  combination  of  the  organic  and  inorganic 
elements  of  the  calculus  occurs  as  time  passes,  density  being  thereby 
increased.  The  organic  basis  is  evidently  a  precipitation  of  a  col- 
loidal material,  probably  mucinous  in  character,  upon  the  teeth,  and 
into  this  the  salts  are  precipitated. 

In  the  analyses  furnished  by  Stevenson  (p.  694)  it  will  be  seen 
that  hardness  is,  in  part  at  least,  due  to  an  increased  proportion  of 
inorganic  elements. 


Fig.  624 


Fig.  625 


Section  of  a  lower  incisor,  with  a  large 
deposit  of  salivary  calculus  impinging 
upon  and  causing  inflammation  of  the 
gum.      (Black.) 


Section  of  an  upper  molar  with  deposit 
of  calculus  on  its  buccal  surface,  causing 
inflammation  and  absorption  of  the  gum 
and  lower  border  of  the  peridental  mem- 
brane and  alveolar  wall.     (Black.) 


Theoretically,  subgingival  calculi,  pyogenic  calculi,  and  hemato- 
genic calculi  formed  within  the  unbroken  pericementum  may  derive 
their  organic  material  from  the  secretions  or  necrotic  tissue  of  the 
part,  and  their  inorganic  material  (largely  phosphate  of  calcium, 
carbonate  of  calcium,  and  sodium  biurate)  from  the  serum  of  the 
blood  (serumal  calculus).  In  the  case  of  simple  subgingival  calculus 
the  saliva  may  play  a  part  by  furnishing  the  necessary  calcium 
salts,  as  claimed  by  Peirce,  but  this  does  not  seem  to  be  absolutely 
proved,  nor  would  it  seem  to  be  necessary;  indeed,  in  certain  cases 
of  pyorrhea  pockets  located  about  lower  incisors  in  which  salivary 


SALIVARY  CALCULUS 


roi 


calculus  might  readily  be  deposited,  and  from  which  both  salivary 
and  serumal  calculus  has  been  thoroughly  removed,  the  serumal 
calculus  has  again  collected  in  quantity,  while  the  salivary  calculus 
has  not  been  redeposited. 

Pathological  Effects  of  Salivary  Calculus. — In  contact  with  the 
mucous  membrane  a  salivary  calculus  excites  first  marginal  gingivitis, 
and  later  deeply  seated  gingivitis  and  its  effects.  There  is  sometimes 
in  this  stage  the  wavy,  gnawing,  uneasy  sensation,  associated  with 
mild  inflammation,  and  the  pulp  being  supplied  with  excess  blood, 
becomes  hyperemic  and  the  teeth  respond  more  readily  to  thermal 
stimuli.  (See  p.  470.)  The  gum  margin  is  inflamed,  and  occasion- 
ally pyogenic  organisms  cause  pus  formation.  The  gum  margin 
recedes  and  coincidently  a  resorption  of  the  alveolar  process  is 
produced.  More  calculus  is  deposited  and  the  process  proceeds 
until  much  of  the  alveolar  support  is  lost.  Microorganisms  no 
doubt  aid  in  the  process. 


Fig.  626 


Fig.  627 


Section  illustration  of  a  heavy  deposit 
of  salivary  calculus  on  a  lower  incisor, 
with  partial  destruction  of  the  alveolus 
of  the  tooth.      (Black.) 


Sectional  illustration  of  lower  in- 
cisor, with  deposit  of  salivary  cal- 
culus less  hea^^'  than  that  shown  in 
Fig.  626,  but  with  greater  destruc- 
tion of  the  alveolus.     (Black.) 


The  tooth  is  thus  progressively  loosened,  first  by  inflammation, 
later  by  loss  of  alveolar  process,  moves  about,  and  a  resultant  mechan- 
ical interstitial  inflammation  of  the  remaining  pericementum  occurs; 
as  a  result  the  membrane  is  thickened  and  the  alveolar  process 
partially  resorbed  (Fig.  624).  As  soon  as  the  aveolar  loss  is  con- 
siderable, infection  usually  occurs  and  suppuration  may  be  grafted 
upon  the  results  of  mechanical  irritation.  Increased  looseness  occurs 
until  the  tooth  drops  out,  unless  mechanically  held  in  place. 


702 


SALIVARY  AND  SERUMAL  CALCULUS 


The  entire  process  may  occupy  but  a  few  years;  in  other  cases 
the  atrophy  of  the  alveolar  walls  is  very  slow.     I  have  recently  seen 


tv 


George  H.  Cushing's  scalers.  The  forms  and  general  character  of  these 
scalers  are  well  shown.  All  the  instruments  except  No.  6  are  intended  to 
be  used  with  the  push  stroke.  Nos.  1  and  2  are  especially  intended  for 
application  to  the  posterior  surfaces  of  lower  incisors ;  they  are  also  admir- 
ably adapted  for  removing  calculus  deposits  below  the  gum  between  molars 
and  bicuspids,  and  from  the  posterior  surfaces  of  the  last  molars.  No.  2 
can  be  passed  quite  to  the  extremity  of  most  roots  with  less  disturbance 
to  the  soft  tissues  than  a  thicker  or  more  rigid  instrument  would  cause. 
Nos.  3  and  4  are  for  removing  deposits  at  and  below  the  gum  between  the 
teeth,  particularly  the  lower  front  teeth.  They  can  also  be  easily  used 
upon  tlie  sides  of  the  roots  of  many  teeth,  being  passed  toward  the  apex 
of  the  root  in  a  line  nearly  or  quite  parallel  with  that  of  the  axes.  No.  5 
is  intended  to  be  passed  between  the  lower  front  teeth  at  or  near  the  gum  and 
then  directly  upward,  to  remove  the  deposits  on  the  proximal  surfaces. 
No.  6  is  a  hoe,  and  is  intended  to  be  passed  quite  to  the  apex  of  the  roots, 
where  a  hoe  is  desired. 


a  case  like  that  shown  in  Fig.  626  on  about  eight 
lower  teeth.  The  patient  had  not  consulted  a 
dentist  for  thirty  years. 

Prognosis. — The  prognosis  of  this  condition 
depends  upon  the  extent  of  alveolar  atrophy. 
If  the  loss  of  support  be  not  so  extensive  as  to 
cause  marked  loosening  of  the  tooth  or  teeth, 
the  teeth  may  be  retained  for  an  indefinite  period 
if  they  receive  constant  prophylaxis.  If  markedly 
loosened  they  must  be  splinted  so  as  to  render 
them  firm.  If  left  unsupported,  the  pericementum 
is  certain  to  degenerate,  owing  to  the  increased 
mobility.  The  alveolar  atrophy  will  continue, 
and  probably  infection  of  the  degenerated  perice- 
mentum occur.  Redeposit  is  almost  certain  unless 
all  morbid  conditions  are  removed  and  extraordi- 
nary precautions  be  taken  as  regards  cleanliness,  which  precautions 
are  difiicult  to  carry  out  without  the  aid  of  a  dentist. 


Fig.  629 


Flat  scaler. 


SALIVARY  CALCULUS 
Fig.  630 


703 

Fig.  631 


E.  C.  Kirk's  scalers  with  dentate  ends,  designed  to  cut  into 
calculus  as  well  as  maintain  the  course  of  the  scaler  upon  the 
root  side. 


Fig.  632 


Fig,  633 


Fig.  634 


No.  3  Scaler, 


Fig.  635 


No.  11  Darby- 
Perry  scaler. 

Fig.  636 


5  S 

Pyorrhea  scalers  Nos.  5  and 
6,  revised  set.  S.  S.  White 
Dental  Mfg.  Co.'s  Catalogue. 
Intended  for  use  between  teeth 
as  well  as  for  pyorrhea. 

Fig.  637 


No.  9  Darby-Perry     No.  35  Darby-Perry     Burton  Lee  Thorp's 
scaler.  excavator.  scalers. 


704 


SALIVARY  AND  SERUMAL  CALCULUS 


Treatment. — The  treatment  may  be  divided  under  three  heads: 
removal  of  deposits,  correction  of  the  effects  of  their  presence,  and 
prevention  of  their  recurrence.  The  sole  means  of  removing  salivary 
calculi  should  be  instrumental. 

It  is  frequently  recommended  that  mineral  or  some  of  the  organic 
acids  be  used  to  soften  the  deposits  or  facilitate  their  removal. 
Anyone  having  seen  a  case  in  which  a  solution  of  sulphuric  acid 
has  been  used  for  this  purpose  needs  no  further  warning  against 
the  application.     Acid  solutions  will  certainly  soften  the  deposits, 

Fig.  638 


Smith  scalers. 

but  at  the  same  time  inevitably  cause  a  roughening  of  the  enamel 
of  the  teeth  by  a  solution  of  the  calcium  salts.  To  be  sure,  the 
acid  does  affect  the  calculus  more  than  it  affects  the  enamel,  but 
the  roughened  surfaces  of  the  latter  not  only  invite  widespread 
deposits  of  fermentable  material,  but  render  certain  the  more  exten- 
sive accumulations  of  calculi  in  the  future.^     After  oral  sterilization 


1  Recently  a  proprietary  preparation  was  offered  me  for  removal  of  stains  with 
assurance  by  the  maker  that  no  injurious  acid  was  present.  I  highly  polished  the 
labial  of  an  extracted  tooth  and  applied  it  for  one  minute.  The  enamel  was  dulled 
and  roughened.  The  preparation  was  acid  to  litmus.  Such  preparations,  if  needed 
in  extreme  cases,  should  be  used  with  great  care. 


SALIVARY  CALCULUS  705 

the  gross  deposits  may  be  removed  by  means  of  large,  sickle-shaped 
scalers,  nearly  all  used  with  a  draw  cut.  The  instruments  should 
have  sharp  edges  and  be  introduced  beneath  the  deposits,  so  that 
the  gum  be  not  unnecessarily  wounded.  The  scaling  should  be 
continued  until  every  surface  which  can  be  cleaned  by  these  instru- 
ments is  perfectly  smooth. 

For  the  approximal  surfaces  of  the  lower  anterior  teeth  the  flat- 
bladed  instruments  should  be  used  with  the  push  cut,  or  that  in 
Fig.  651  with  the  draw  cut.  Younger's  pyorrhea  scalers  are  very 
useful  (Fig.  649).    Thorpe's  scalers  are  useful  (Fig.  637.) 

For  the  removal  of  associated  subgingival  calculus  not  too  deeply 
placed  beneath  the  gum  a  No.  35  Darby-Perry  excavator  is  of  almost 
universal  utility.  It  is  used  with  the  draw  cut  for  the  most  part. 
A  pair  of  them  may  be  employed  and  made  safe-sided  by  rounding 
one  edge  if  desired,  to  avoid  injury  of  the  gum  margin.  The  back 
of  the  instrument  may  be  sharpened  to  an  edge  for  a  push  cut. 
Smith's  file  scalers  (Fig.  638)  are  useful  for  rubbing  o£F  calculus  that 
can  not  be  scaled  off  as  a  flake.     All  of  the  calculi  visible,  and  all 

Fig.  639 


Moose-hide  wheels. 

that  can  be  detected  by  their  roughness,  are  thoroughly  detached 
and  scraped  away  with  instruments.  The  surfaces  of  the  teeth 
are  next  cleansed  with  pumice  made  into  a  paste  with  glycerin  to 
prevent  spattering,  and  with  a  few  drops  of  hydrogen  dioxid  for 
antisepsis;  flavoring  matter  or  cologne  may  be  added.  The  paste 
is  applied  to  the  surfaces  of  the  teeth  with  rubber  cups,  or  Abbott's 
or  Robinson's  brush  wheels,  which  are  used  to  cleanse  the  labial, 
buccal,  and  such  lingual  faces  of  the  teeth  as  they  will  reach  (Figs. 
640  to  644).  The  gum  should  not  be  injured.  When  using  brush 
wheels  it  is  well  to  apply  the  brush  to  a  point  aw^ay  from  the  gum 
and  spread  the  bristles  sgainst  the  tooth  as  it  is  carried  toward  the 
gum.  The  second  brush  in  Fig.  640  is  the  best  for  the  labial  sur- 
face and  lingual  of  bicuspids  and  molars,  and  the  third  one  for  the 
lingual  of  lower  incisors.  The  lingual  surfaces  of  upper  and  lower 
incisors  are  cleansed  with  moose-hide  wheels  and  wheel  brushes;  a 
finishing  bur^  is  useful  in  the  removal  of  thinly  distributed  hard 

1  Guilford  Lectures. 
45 


706 


SALIVARY  AND  SERUM  A  L  CALCULUS 


calculi  on  lingual  and  occlusal  surfaces,  especially  in  the  mouths 
of  smokers. 

The  approximal  surfaces  of  the  teeth  are  cleansed  with  fine  linen 
tape  or  flat  floss  silk  charged  with  the  pumice  paste.  More  inac- 
cessible parts  require  the  use  of  an  orange-wood  point  mounted  in 
a  Jack  porte-polisher  (Fig.  645).  It  is  advisable  to  repeat  the 
polishing  with  precipitated  chalk  and  the  same  carriers.  When 
prophylaxis  is  frequent  chalk  is  a  sufficient  abrasive  except  perhaps 
with  the  wood  point. 

Fig.  640 

■       "" 


Abbott  brush  wheels. 


Fig.  641 


Fig.  642 


^  J  (^.M  .J  ^  m.  J 


After  cleansing,  the  associated  gingivitis  should  be  reduced  and 
the  parts  kept  sterilized  while  healing  by  means  of  an  antiseptic 
astringent  mouth  wash.     (See  Gingivitis.) 

If  desired,  the  operation  may  be  divided,  the  gross  deposits  and 
subgingival  calculus  being  removed  at  the  first  sitting.  After  a  few 
days'  use  of  the  mouth  wash  the  stains  and  bacterial  plaques  upon 
the  teeth  and  any  overlooked  deposits  may  be  removed.  Tincture 
of  iodin  painted  over  the  teeth  brings  the  deeper  stains  of  the 
collection  into  prominence,  as  does  also  a  solution  of  potassium 
permanganate. 

Register  states  that  a  forcible  spray  of  1  per  cent,  hydrogen  dioxid 
used  after  the  application  of  tincture  of  iodin  will  soften  the  stains 
and  render  them  more  readily  removable.  The  iodin  is  also  rather 
germicidal. 


SALIVARY  CALCULUS 


707 


Prophylaxis. — The  smoother  the  surfaces  of  the  teeth  are  made, 
the  longer  the  redeposition  of  calcuh  will  be  delayed.     Black  sug- 


FiG.  643 


Fig.  644 


Fig.  645 


gests  the  use  of  the  ordinary  chip  syringe  and  plain 
water,  a  forcible  stream  being  accurately  used  to 
wash  away  the  agglutinin.  As  a  means  of  calculus 
prevention  it  should  be  valuable. 

It  is  a  wise  measure  to  cleanse  the  teeth  before 
any  long  series  of  operations  is  undertaken,  and 
as  a  prophylactic  measure  in  the  combat  with 
caries  and  pyorrhea  alveolaris  the  operation 
should  be  frequently  performed.  Indeed,  the 
teeth  should  be  cleansed  frequently,  so  that  it 
may  not  be  necessary  to  remove  actual  salivary 
calculus,  except  in  those  cases  in  which  it  col- 
lects with  abnormal  rapidity.  A  stick  in  a  metal 
handle  for  self-prophylaxis  is  useful  if  the  patient 
will  use  it.     (See  p.  442.) 

In  cases  of  very  rapid  recurrence  of  salivary 
deposits,  evidence  of  an  associated  systemic 
condition  should  be  sought.  In  this  direction 
sialosemeiology  and  urinalysis  may  develop  data 
worthy  of  attention.  The  systemic  condition,  if 
recognizable,  should  receive  appropriate  treat- 
ment. If  not  recognizable,  the  method  suggested 
by  Black  of  reducing  the  quantity  of  food  and 


Dj 


Hiiinni 


Jack  porte-polisher. 


708 


SALIVARY  AND  SERUMAL  CALCULUS 


the  thorough  mastication  of  such  as  is  taken,  may  be  conjoined 
with  the  occasional  use  of  Epsom  salt,  if  further  needed  as  sug- 
gested.    (See  p.   697. "i 

SUBGINGIVAL  CALCULUS. 

By  subgingival  calculus  is  meant  that  form  of  deposit  which 
occurs  beneath  the  free  gum  margin  and  between  it  and  the  tooth. 
The  deposits  consist  of  small  scales  or  granules,  usually  quite  smooth 
and  much  darker   (olive  green)   than   salivary  calculi    (Fig.   646). 

Fig.  646 


A,  subgingival  calculus;    B,  receding 
pericementum.     (Black.) 


Resorption  of  the  septum  of  bone  and 
recession  of  the  gum  between  the  central 
and  lateral  incisors,  caused  by  deposits  of 
serumal  calculus  under  the  gingivae. 
(Black.) 


Composition. — They  consist  mainly  of  calcium  phosphate  combined 
with    undetermined    organic    substances.     (See  pp.   694  and  697.) 


Fig.  648 


The  alveoli  irreparably  destroyed  by  calcic  inflammation.     (Black.) 

Cause  and  Pathology. — It  is  probable  that  some  degree  of  marginal 
gum  irritation  first  occurs,  though  many .  cases  of  an  apparently 
healthy  gum  with  a  scale  of  calculus  beneath  it  are  seen.  Whether 
the  irritation  arises  through  fermentations  about  the  unclean  necks 


SUBGINGIVAL  CALCULUS  709 

of  the  teeth  or  as  the  result  of  an  effort  upon  the  part  of  the  gum 
margin  to  eHminate  waste  products  from  the  system  is  not  absolutely 
certain. 

The  theory  most  tenable  is  that  uncleanliness  exists;  fermentation 
of  the  mixed  marginal  collection  and  altered  gum  secretion  contain- 
ing a  precipitable  organic  material,  occurs,  the  gum  secretion  con- 
taining also  calcium  salts;  these  are  precipitated,  forming  a  calculus. 
Fig.  297  shows  a  calculus  on  an  unerupted  tooth  root,  showing  that 
the  blood  contains  the  elements  necessary  for  its  formation  under 
localized  irritation. 

Talbot  has  shown  that  a  natural  pocket  may  exist  at  some  aspect 
of  the  gingival  space  which  is  capable  of  harboring  collections  of 
foreign  material.  The  normal  gum  margin  closely  approximates 
the  tooth  and  has  an  apparent  protective  influence  over  the  portion 
it  covers.  For  some  reason,  such  as  a  lack  of  normal  friction  or 
the  presence  of  microbic  plaques  just  above  it,  the  gum  may  lose  its 
normal  tone  and  the  calculus  deposition  be  favored.  Its  secretion 
is  also  probably  altered  in  quality. 

Effects  and  Symptoms. — The  direct  effects  are  exerted  upon  the  gum 
margin.  The  mechanical  irritation  may  cause  the  gum  and  alveolar 
process  to  undergo  resorption,  the  calculus  being  exposed. 

At  times  this  resorption  is  accompanied  by  evident  marginal 
inflammation,  at  others  the  gum  margin  has  a  normal  color,  but  the 
resorbing  portion  is  sharply  defined  by  a  fine  line  (or  crease)  from 
the  normal  gum  tissue,  especially  at  the  interdental  septum.  In  a 
more  advanced  stage  this  demarked  portion  appears  sunken  or 
atrophied,  and  may  have  a  sort  of  semihyalin  redness  characteristic 
of  the  inflammation.  At  times  the  gum  m.argin  appears  everted 
(Fig.  647  n).  If  the  deposit  occur  on  only  one  side  of  a  root  the  gum 
resorption  may  be  confined  to  that  side. 

The  lingual  root  of  an  upper  molar  is  often  exposed  for  a  con- 
siderable portion  of  its  length  by  successive  deposits  of  calculi.  The 
same  is  true  in  other  situations,  notably  upon  the  labial  surface  of  a 
lower  incisor.  This  might  be  called  a  form  of  marginal  phagedenic 
gingivitis. 

If  the  deposit  be  generally  distributed  about  the  neck  of  the  tooth 
the  resorption  is  more  equalized. 

In  some  cases  the  bifurcation  of  roots  may  be  exposed  and  calculi 
deposit  in  that  situation. 

In  some  cases  the  gum  margin  becomes  simply  atonic  or  passively 
congested  and  is  pushed  away  from  the  teeth  by  large  masses  of  the 
calculus,  which  undergo  lateral  accretion.  It  appears. as  a  flabby, 
thickened,  loosened  gum  margin,  which  readily  draws  about  the 


710 


SALIVARY  AND  SERUMAL  CALCULUS 


necks  of  the  teeth  if  the  calculus  be  removed.     I  have  noted  this 
in  cases  of  suboxidation  with  bluish  lips,  and  in  renal  insufficiency. 


Fig.  649 


5      6 


Fig.  650 


9  10  II     12  13  14  15 

Younger's  new  set  of  pyorrhea  instruments.     (Revised  by  Dr.  Robert  Good.) 

Fig.  651 


Tompkins'  pyorrhea  scalers. 

Finally,  pyogenic  infection  may  occur  about  the  calculus  and  the 
symptoms  of  pyorrhea  alveolaris  be  implanted.  When  this  is  estab- 
lished, calculi  may  be  deposited  farther  up  the  side  of  the  root.     This 


HEMATOGENIC  CALCULUS  711 

pathology  often  precedes  the  condition  of  pyorrhea  alveolaris  which 
may  supervene  if  pyogenic  organisms  enter  the  area. 

Treatment. — The  calculus  should  be  removed  by  means  of  dehcate 
scalers  used  with  either  the  push  or  draw  cut,  as  most  convenient, 
after  which  astringent  antiseptic  mouth  washes  should  be  prescribed. 
The  subsequent  frequency  of  removal  of  causes  by  oral  prophylaxis  is 
of  great  importance.  Figs.  649,  650,  and  651  show  convenient  forms 
also  useful  for  the  deeper  pyorrhea  pockets.  In  most  cases  healing 
is  spontaneous  even  without  medication,  but  often  the  washes  are 
of  advantage.  If  pyorrhea  be  present  on  any  tooth  it  is  to  be  con- 
sidered separately. 

PYOGENIC  CALCULUS. 

Pyogenic  calculus  is  that  form  of  serumal  calculus  which  is  deposited 
at  parts  of  the  tooth  root  over  which  pus  more  or  less  continually 
flows.     Talbot  has  shown  that  pus  is  rich  in  calcium  phosphate. 

In  chronic  apical  abscess  the  root  end  may  become  encrusted  with 
it,  and  in  those  cases  in  which  apical  abscess  discharges  along  the 
pericemental  tract  it  is  common  to  find  over  the  area  fine  granular 
deposits  which  vary  in  color  from  a  light  yellow  to  a  reddish  brown. 

The  same  is  true  of  active  pyorrhea  pockets. 

This  calculus  prevents  the  healthy  apposition  of  the  gum  tissue 
to  the  roots,  probably  because  of  its  irritant  and  infective  nature 
(Figs.  558  and  652). 

Treatment. — All  such  calculi  should  be  removed  by  whatever 
means  possible,  which  may  necessitate  scraping  the  root  end  or 
its  side,  or  even  the  amputation  of  the  apical  end  of  the  root.  In 
some  cases  25  per  cent,  sulphuric  acid  or  Tartasol  may  dissolve 
it.     (See  pp.  622  and  738.) 

HEMATOGENIC   CALCULUS   (Syn.  SANGUINARY  CALCULUS). 

This  form  of  serumal  calculus  occurs  in  the  so-called  gouty  peri- 
cementitis, a  form  of  pericemental  abscess. 

It  may  occur  in  the  abscence  of  apical  abscess  or  a  primary  pyorrhea 
alveolaris,  and,  therefore,  at  points  not  acted  upon  by  saliva  or  pus; 
hence  it  must  be  deposited  by  the  blood  through  the  lymph. 

Miller^  has  offered  satisfactory  evidence  of  this  in  a  description  of 
a  case  of  impacted  cuspid  well  embedded  in  the  bone,  and  not  in 
any  way  exposed  to  either  saliva  or  pus  influence  except  that  at  a 

1  Dental  Cosmos,  August,  1901. 


712  SALIVARY  AND  SERUMAL  CALCULUS 

point  over  the  cusp  the  gum  underwent  suppuration  for  a  short  time. 
The  crown  had  undergone  resorption,  showing  local  irritation,  and 
an  olive-green  calculus  had  formed  upon  the  middle  third  of  the 
root.  Cases  of  pericemental  abscess  have  been  noted  opening 
upon  the  gum  face  and  presenting  dark  green  calculi  upon  the  root 
in  that  situation  (Fig.  297).     (See  Pericemental  Abscess.) 

Peirce  found  in  such  deposits  a  proportion  of  sodium  urate  as 
shown  by  the  murexid  test  and  the  cases  associated  with  goutiness 
of  the  patient. 

While  such  deposits  may  not  cause  immediate  irritation,  they  may 
in  time  excite  inflammation  and  necrosis  of  tissue,  resulting  in  a 
discharge  of  glairy  material  representative  of  the  condition.  This 
form  of  dental  disease  will  be  further  discussed. 


CHAPTER  XXIV. 
PYORRHEA  ALVEOLARIS. 

General  Considerations. — The  term  pyorrhea  alveolaris  means  a 
flow  of  pus  from  a  pus  pocket  located  between  the  root  of  the  tooth 
and  the  alveolar  wall  at  the  lateral  aspect  of  the  root.  Apical  and 
lateral  abscess  from  gangrenous  pulp  or  perforation  are  excluded.  The 
alveolar  wall  may  be  more  or  less  intact  and  either  be  exposed  and 
necrotic  or,  as  more  generally  the  case,  be  still  covered  with  its 
internal  periosteum,  which  is  the  remains  of  the  pericementum. 
In  some  cases  the  bone  has  disappeared  and  the  gum  tissue  forms  the 
outer  covering.  Pyorrhea  alveolaris  always  involves  the  considera- 
tion of  marginal  and  deeply  seated  gingivitis,  but  these  need  not 
necessarily  be  pyorrhea.  It  is  therefore  somewhat  difficult  to  differ- 
entiate from  gingivitis  proper,  as  any  form  of  gingivitis  may  later 
assume  the  characteristics  of  pyorrhea  owing  to  infection. 

In  a  general  way  pyorrhea  alveolaris  may  be  diagnosticated  when 
there  is  a  progressive  gum  pocket  formed  at  the  expense  of  the 
lateral  portion  of  the  pericementum,  and  the  tooth  becomes  pro- 
gressively loosened.  Usually  calculi  and  a  pus  flow^  ar<e  found,  but 
in  some  cases  neither  are  much  in  evidence. 

The  disease  ceases  spontaneously  with  the  loss  of  the  teeth,  though 
the  alveolar  process  is  further  resorbed  as  after  any  extraction. 

Causes. — It  seems  that  anything  which  may  induce  a  gingivitis 
may  initiate  the  process  when  infection  is  added  of  a  character  that 
will  destroy  the  pericementum  and  produce  the  pocket  at  its  expense. 
Therefore  the  causes  of  gingivitis  or  even  of  non-septic  pericementitis 
are  the  primary  causes  of  pyorrhea  alveolaris  (see  pp.  665,  674,  and 
682,  etc.). 

The  gingivitis  itself  is  the  proximate  predisposing  cause  and  the 
specific  infection  is  the  proximate  exciting  cause.  It  is  obvious  that 
these  are  difficult  of  exact  differentiation,  i.  e.,  it  is  difficult  to  say 
when  gingivitis  ceases  to  be  such  and  becomes  a  pyorrhea,  but  when 
the  pocket  is  established  the  case  may  practically  be  called  a  pyor- 
rhea, and  is  treated  as  such.  From  a  prophylactic  standpoint  it  is 
wise  to  remove  all  causes  of  gingivitis  as  it  is  apt  to  lead  to  a  pyorrhea. 

The  causes  of  marginal  gingivitis  are  mostly  obvious  and  have 
been  discussed.  (See  p.  674.)  The  causes  of  deeply  seated  gingivitis 
apart  from  pyorrhea  are  more  obscure,  but,  as  stated  in  the  dis- 

(713) 


714  PYORRHEA  ALVBOLARIS 

cussion  (p.  682),  are  either  the  more  deeply  acting  causes  of  marginal 
gingivitis  or  are  due  to  local  or  systemic  causes  which  produce  a 
more  or  less  profound  pericementitis  or  gingivitis  apart  from  the 
alveolar  pockets,  and  which  have  a  tendency  to  cause  inflammatory 
degeneration  of  the  soft  tissues  and  to  produce  a  resorption  of  the 
bony  tissue,  thus  predisposing  the  soft  tissues  to  the  local  action  of 
bacteria,  or,  in  other  words,  lessening  their  resistance  to  bacteria. 

Aside  from  inflammatory  conditions  actually  produced  by  sys- 
temic conditions,  the  pericementum  may  be  influenced  by  a  lack  of 
proper  nutrition,  as  in  anemia  or  neurasthenia  or  some  form  of 
systemic  drain,  as  peripheral  nutrition  is  evidently  lessened  in  such 
states,  and  tissues  seem  more  subject  to  infection.  The  opsonic 
index  is  probably  lowered.     (See  p.  62.) 

Investigations  as  to  cause  have  proved  uncertain  in  so  far  as  the 
determination  of  a  specific  bacterium  is  concerned. 

Galippe  and  Malassez,  Miller,  Black,  Talbot,  Goadby,  Younger, 
Cook,  and  others  have  all  failed  to  definitely  isolate  such  a  specific 
bacterium.  The  closest  approach  to  a  demonstration  yet  made  was 
the  determination  by  Kirk  of  the  presence  of  a  pure  culture  of  the 
Diplococcus  pneumoniae  in  a  few  cases  of  freshly  opened  pericemental 
abscesses  (which  see). 

The  investigations  of  Goadby,  however,  do  not  confirm  this  as  a 
cause  of  pyorrhea  alveolaris  in  general,  but  rather  point  to  the  prob- 
ability that  the  cause  may  be  found  among  other  oral  bacteria, 
possibly  thread  forms  or  some  of  the  blastomycetes.  Talbot  believes 
the  ordinary  pyogenic  cocci  to  be  the  cause  of  the  pus  production. 

Recently,  M.  T.  Barrett,^  working  with  Allen  J.  Smith,  M.D., 
has  found  in  the  pus  of  46  straight  cases  of  pyorrhea  actively  motile 
endamoebse  (probably  Prowazek's  endamoeba  buccalis  (Barrett)). 
Of  ten  apparently  healthy  mouths  used  as  controls  close  .examination 
revealed  three  with  pockets  with  endamoebse  in  the  contents  and 
seven  without  pockets  or  endamoebse.  The  local  treatment  with 
an  amoebacide  (emetin  hydrochlorid,  ^  to  1  per  cent.,  in  normal 
saline  solution  was  effective  on  several  successive  days.  He  refers 
to  a  fiagellate  protozoon  and  a  ciliated  one  as  found  occasionally. 
Whether  this  is  the  exciting  cause  of  pyorrhea,  Barrett  has  not  yet 
definitely  claimed.  Chiavaro^  also  found  the  endamoeba  buccalis, 
but  regards  it  as  non-pathogenic. 

Curtis^  believes  obstinate  cases  of  the  disease  to  be  either  caused 
by  or  aggravated  by  tertiary  syphilis.  He  bases  his  belief  upon 
observations  of  fresh  blood  which,  he  states,  upon  the  authority  of 
Dr.  Robert  L.  Watkins  (New  York  City),  contains  syphilitic  spores. 

.    1  Dental  Cosmos,  August,  1914. 
2  Ibid.,  September,  1914.  s  ibid.,  1901. 


GENERAL  CONSIDERATIONS  715 

"Egg-skin"  eschar  is  the  oral  pathognomonic  sign. 

According  to  Curtis,  the  local  infection  in  nearly  all  cases  is  of 
so  mixed  a  type  as  to  render  it  at  present  uncertain  whether  the 
liquefaction  of  the  peridental  membrane,  etc.,  is  due  directly  to 
the  pyogenic  organisms  present  in  the  pus  formed  or  to  other  oral 
bacteria  of  uncultivable  type  which  may  initiate  the  process,  after 
which  pyogenic  organisms  may  enter  and  form  pus.  The  fact  that 
pyorrhea  alveolaris  is  seldom  found  fully  established  before  thirty 
years  of  age,  but  is  common  after  that  period,  and  that  it  occa- 
sionally occurs  in  youth  or  even  in  childhood  associated  with  some 
pronounced  systemic  state  or  disease,  strongly  indicates  a  systemic 
factor  in  the  more  pronounced  forms  of  the  disease. 

The  type  of  teeth  affected  is  usually  that  of  the  narrow-necked 
variety  in  which  the  angle  formed  by  the  gum  and  tooth  is  less 
accessible  to  the  brush  and  friction  of  mastication.  This  leads  both 
to  formations  of  calculus  and  to  the  retention  of  infective  material. 

In  brief,  it  may  be  stated  that  the  infectious  nature  of  pyorrhea 
alveolaris  is  becoming  more  established  though  not  yet  fully  scien- 
tifically proved,  and  that  the  causes  probably  require  a  local  predis- 
position for  their  action,  though  it  may  be  that  continued  infection 
is  a  sufficient  cause.  This  local  predisposition  may  be  the  outcome 
of  local  sources  of  irritation  and  degeneration  alone  or  be  produced 
by  waste  products  floating  in  the  blood  stream,  etc.,  or  by  a  lack  of 
nutrition  due  to  general  causes.  Clinically  in  support  of  a  local 
origin  it  may  be  observed  that  oral  conditions  leading  up  to  pyorrhea 
are  seen  existing  for  years  previous  to  a  fully  established  and  active 
condition.  The  presence  of  such  a  state  therefore  must  not  lead 
one  hastily  to  assume  that  it  is  of  necessity  a  disease  of  systemic 
origin,  and  at  present  the  systemic  sequels  of  pyorrhea  seem  of  more 
importance  than  its  possible  systemic  origin.  In  observing  mouths 
at  all  times  one  should  look  ahead  from  all  forms  of  gingivitis  or  causes 
liable  to  produce  it  to  a  possible  future  pyorrhea  and  take  measures 
to  prevent  it.     (See  pp.  665,  674,  and  682.) 

Clinically,  fully  established  cases  of  pyorrhea  alveolaris  may  be 
divided  into  three  classes:  (1)  Cases  associated  with  a  primary 
gingivitis  and  with  the  formation  of  hard,  scaly,  dark,  annular 
calculi  beneath  the  gum  margin  (subgingival  calculus),  the  pockets 
not  usually  extending  far  beyond  the  deposits;  (2)  cases  beginning 
with  a  marginal  gingivitis  and  apparently  not  dependent  upon  the 
association  with  calculus,  though  frequently  complicated  by  it; 
(3)  cases  having  an  apparent  origin  at  some  point  between  the 
gingival  margin  and  the  apical  tissue,  the  gingival  margin  at  first 
being  apparently  intact. 


716  PYORRHEA  ALVEOLARI'S 

It  is  probable  that  the  infecting  agents  in  these  types  differ  in 
their  nature,  or  that  in  the  event  that  they  may  be  proved  to  have 
a  similar  origin  the  tissues  react  differently  to  them,  either  partially 
resisting  them,  forming  calculus  as  a  result  of  the  irritation,  or 
rapidly  giving  way  to  them,  permitting  a  deep  action. 

In  the  abscence  of  known  causes  the  conditions  may  be  divided 
according  to  their  clinical  expressions. 

In  the  consideration  a  pus  flow  due  to  apical  abscess,  lateral  abscess 
upon  a  perforation,  or  that  due  to  obvious  salivary  calculus  (for 
these,  see  under  proper  headings),  also  simple  gingivitis  or  deeply 
seated  gingivitis,  not  resulting  in  the  clinical  feature  of  pyorrhea  as 
defined,  are  excluded. 

PYORRHEA  AVEOLARIS  BEGINNING  AS  A  MARGINAL  GINGI- 
VITIS AND  ASSOCIATED  WITH  SUBGINGIVAL  CALCULUS. 

Causes. — The  causes  of  this  condition  are  those  predisposing  and 
exciting  causes  of  marginal  gingivitis  which  have  been  described. 
(See  p.  674.)  Several  local  factors  have  to  be  considered  in  this 
connection:  (1)  The  marginal  infection;  (2)  the  irritative  effects  of 
any  calculus  that  may  be  formed;  (3)  the  deep  infection  by  pyogenic 
organisms;  (4)  the  modification  of  the  progress  of  the  disease  by  the 
attendant  loosening  of  the  teeth  and  death  of  the  pulp. 

Clinical  History,  Pathology,  and  Symptoms. — There  is  usually  an 
unclean  condition  of  the  teeth;  infection  exists  either  in  tenacious 
films  of  bacteria  attached  to  the  necks  of  the  teeth  and  requiring 
reasonably  close  observation  for  their  detection,  or  in  masses  of 
detritus  readily  noticeable.  Subgingival  calculus  is,  as  a  rule, 
obviously  present  (Fig.  657). 

The  gum  margin  may  be  atrophied  or  be  inflamed;  or  it  may  have 
a  fairly  normal  appearance.  When  the  gum  margin  is  pressed  upon, 
pus  may  be  squeezed  out  in  variable  quantity. 

It  is  assumed  that  the  local  infection  brings  about  the  deposit  of 
mucous  exudates  rich  in  calcium  salts  at  a  point  beneath  the  gum 
margin,  and  that  formation  of  subgingival  calculus  occurs,  followed 
by  pyogenic  infection  and  pus  formation. 

The  gum  may  now  be  resorbed  either  with  apparently  normal 
bulk  or  the  margin  may  be  everted  and  thickened  into  a  cord-like 
margin  which  is  either  of  normal  color  or  inflamed;  the  shrinkage 
of  the  gum  causes  the  exposure  of  the  calculus  (Fig.  646).  In  this 
manner  the  bifurcations  of  the  roots  may  be  uncovered  and  calculi 
be  deposited  in  that  situation.  The  resorption  may  only  be  con- 
fined to  one  side  of  a  root  and  be  the  result  of  several  successive 


PYORRHEA  ALVEOLARIS  AS  A   MARGINAL  GINGIVITIS     717 

depositions  which  may  remain  when  the  gum  recedes,  or  which  may 
be  removed  and  again  be  deposited.  In  this  way  the  side  of  the  root 
may  be  exposed  nearly  to,  and  in  some  cases  quite  to,  the  apex. 

Fig.  652 


Serumal  calculus,  showing  stalactite-like  formations.     (Talbot.) 

The  destruction  of  the  tissues  may  assume  several  forms.  In 
certain  mouths,  especially  in  neurasthenic  and  anemic  •  patients,  a 
viscous  material  may  accumulate  upon  the  necks  of  teeth  or  exposed 

Fig.  653 


Destruction  of  pericementum,  bone,  and  gum  over  buccal  root  of  a  molar. 


roots;  and  the  pericementum,  bone,  and  gum  may  rapidly  inflame 
and  disappear,  leaving  the  roots  exposed  to  collect  more  of  the 
material,  while  pus  may  not  be  much  in  evidence. 


718  PYORRHEA   ALV SOLARIS 

The  resorption  may  occur  as  shown  in  Fig.  654,  or  the  gum  may 
be  spUt  and  the  destruction  follow  the  length  of  the  root  on  one  side 
only  until  even  the  apex  is  reached  (Fig.  653). 

The  tooth  may  be  loose  or  firmly  attached  by  the  remainder  of  the 
pericementum.  This  is  especially  true  of  those  teeth  having  very 
narrow  necks,  in  which  the  roots  describe  a  prominent  curve  just 
above  the  cervix. 

Fig.   054 


Res6rption  of  gum  over  palatal  root  of  an  upper  molar,  associated  with  but  trifling 
deposit  of  calculus,  but  the  root  is  covered  with  a  viscid  deposit.  Aged  thirty-two 
years.  Patient  neurasthenic  and  of  tuberculous  diathesis.  Condition  in  1904.  Tooth 
lost  in  1907.    In  1912  several  other  teeth  were  lost.    In  1914  several  more  have  gone. 

Fig.  654  is  a  model  of  the  lingual  side  of  the  right  upper  teeth 
undergoing  the  former  process.  The  left  upper  posterior  teeth  and 
the  lower  incisors  have  also  been  lingually  affected.  There  is  but 
little  calculus,  but  the  viscous  material  is  quite  abundant,  black 
stain  is  present,  and  dental  caries  is  rife.  The  patient  has  been 
anemic  and  neurasthenic  for  years,  and  one  lower  molar  has  been 
removed  for  resorption  of  the  apices  of  the  roots  associated  with 
looseness.  Many  teeth  have  been  lost.  The  patient  is  unable  to 
perform  an  exact  dental  toilet  and  does  not  employ  the  dentist  as 
she  should. 

In  such  cases  the  pus  pocket  may  not  be  deep  and  the  pus  formed 
may  readily  be  washed  away.  Such  cases  present  some  resemblance 
to  simple  gingivitis  and  might  be  so  classed  if  there  were  no  pus  flow. 
Instead  of  this  the  pericementum  may  be  progressively  destroyed 
by  suppuration  and  the  gum  margin  remain  practically  intact.  In 
these  cases  the  pus  flow  is  more  abundant,  a  deep  pocket  is  formed, 
extending  a  third  or  even  two-thirds  or  more  of  the  length  of  the 
root  (Fig.  655).  It  is  common  to  find  beads  of  calculus  deposited 
along  the  side  of  the  root  and  presumably  of  serumal  origin.  (See  p. 
708.)  The  cementum  being  deprived  of  nutrition,  its  minute  nutri- 
tional openings  or  openings  containing  fibers  harbor  bacteria. 

These  inflammatory  disturbances  necessarily  involve  deeply 
seated  gingivitis  or  infiltration  of  leukocytes  into  the  interstitial 


PYORRHEA   ALVEOLARIS  AS  A   MARGINAL  GINGIVITIS     719 

connective  tissue  of  the  gum.  As  pointed  out  by  Talbot,  resorption 
of  various  kinds  and  at  times  constructive  changes  accompany  such 
an  inflammation.  (See  Deeply  Seated  Gingivitis.)  Endarteritis  is 
also  noted.  These  results  are  noted  in  connection  with  this  variety 
of  pyorrhea  alveolaris.  In  the  early  stages  of  the  disease  the  probe 
usually  fails  to  discover  uncovered  alveolar  bone,  although  it  may  do 
so.  If  not  uncovered  its  loss  is  due  to  resorption;  if,  however, 
necrotic  and  bare  alveolar  bone  be  found,  it  is  undergoing  a  molecular 
necrosis  under  the  influence  of  the  pyogenic  organisms. 


Fig.  655 


Pyorrhea  pockets.  Mesial  root  of 
molar  largely  denuded.  Treated  by 
amputation.     (Price.) 


Section  of  an  upper  incisor,  showing  at 
a,  a,  a  deposit  of  serumal  calculus  within 
the  free  margin  of  the  gum.     (Black.) 


In  some  cases  the  pericementum  may  be  destroyed  at  the  cervical 
third  of  the  root,  the  aveolar  process  may  be  resorbed  on  its  inner 
surface,  and  an  accompanying  constructive  irritation  may  cause 
the  deposition  of  bone  upon  the  outer  aspect  of  the  alveolar  process; 
the  gum  margin  is  also  thickened  by  cell  proliferation.  The  con- 
dition imparts  the  appearance  of  hypertrophy  of  the  gum  and  gum 
margin  (Fig.  657).  The  inflammation  of  the  pericementum  may 
become  general  and  the  attendant  swelling  forces  the  tooth  into 
malocclusion  with  its  antagonist.  The  mechanical  factor  is  now 
introduced  and  the  extrusion  increases  gradually  or  even  rapidly. 
Sometimes  such  teeth  can  be  ground  one-eighth  inch  before  removing 
the  excess  occlusion.     Such  constant  pounding  is  deadly. 

When  about  one-half  or  more  of  the  root  has  been  stripped  of 
pericementum  and  deprived  of  alveolar  support,  looseness  and 
extrusion  of  the  tooth  become  marked. 

The  advance  of  the  disease  now  becomes  more  rapid;  the  undue 
mobility  and  malocclusion  of  the  tooth  excite  an  inflammatory 
reaction  beyond  the  directly  infected  part;  so  that  soreness  and 
looseness  are  further  increased.  Extraction  at  the  later  stages 
reveals  a  thickened  apical  pericementum  as  the  sole  attachment  to 


720 


PYORRHEA  ALVEOLARIS 


the  bone.  After  the  looseness  of  the  tooth  becomes  marked,  the 
pulp  of  the  tooth  undergoes  hyperemia  changes,  reacts  to  thermal 
stimuli,  and  is  often  killed  by  strangulation  of  its  vacuolar  supply. 
Pulp  nodules  often  are  formed  before  its  death.  Reflex  symptoms 
may  occur  at  this  stage  when  the  pus  pocket  approaches  the  apex. 
(See  Pulpitis.)  Infection  of  the  dead  or  practically  dead  pulp 
readily  occurs  via  the  pocket  (see  Fig.  653),  and  septic  apical  perice- 
mentitis arises.  The  symptoms  of  the  latter  condition  are  modified, 
according  to  the  facility  with  which  the  pus  finds  vent  along  the 
pyorrhea  pocket.  In  some  cases  pericemental  abscess  becomes 
associated.  The  disease  proceeds  until  the  affected  tooth  or  teeth 
are  cast  out,  the  alveolar  walls  having  been  largely  absorbed,  and 


Fio    657 


Fig.  658 


Section  of  an  upper  incisor,  showing 
destruction  of  tlie  peridental  membrane 
and  eversion  of  the  alveolar  wall,  with 
thickening  of  its  border:  a,  serumal  cal- 
culus; b,  thickened  border  of  the  alveolar 
wall;  c,  pus  cavity.    (Black.) 


Section  of  an  upper  molar  with  its 
alveolus,  etc.,  showing  deposit  of  serumal 
calculus  under  the  gingival  borders:  a,  a, 
serumal  calculus.     (Black.) 


the  pericementum  largely  destroyed.  The  remainder  of  it  is  usually 
swollen.  The  disease  ceases  with  the  loss  of  the  affected  teeth, 
leaving  a  flattened  or  absent  alveolar  ridge  covered  by  a  mass  of 
more  or  less  spongy  gum  tissue. 

The  duration  of  this  disease  may  be  months  or  years,  and  a  number 
of  teeth  may  be  affected  at  once.  A  general  subcatarrhal  condition 
of  the  mouth  usually  attends  the  disease.  The  presence  of  pus 
often  imparts  to  the  breath  a  peculiar,  sweetishly  fetid  odor  which 
may,  however,  be  masked  by  an  odor  of  putrefaction  (pigstye  or 
sewer-gas  odor). 

.  It  is  often  the  case  that  the  shifting  of  pyorrhetic  teeth  permits 
the  other  teeth  to  move  into  a  position  in  which  they  malocclude. 
This  brings  in  a  mechanical  cause  of  interstitial  gingivitis,  which, 


PYORRHEA  ALVEOLARIS  AS  A   MARGINAL  GINGIVITIS     721 

with  the  existing  infection,  brings  other  teeth  into  the  pyorrhetic 
state. 

Associated  Abscess. — In  a  number  of  cases  of  deep  pyorrhea  pockets 
an  infection  of  the  aveolar  structure,  or,  at  least,  of  the  tissue  remain- 
ing over  the  deepest  portion  of  the  pocket,  may  occur,  and  an  abscess 
form  which  discharges  by  a  fistula  through  the  labial  or  lingual 
aspect  of  the  gum.  It  is  to  be  regarded  as  an  abscess  secondary 
to  a  primary  pyorrhea  alveolaris.  The  passage  of  a  silver  probe 
through  the  two  sinuses  at  once  w^ill  reveal  this  (Fig.  660).     In  a 

Fig.  659 


Inflammation  of  pericementum,  endarteritis  obliterans.    Talbot's  case.    (Latham.) 


tooth  treated  for  apical  abscess  such  a  pyorrhea  pocket  existed,  and 
doubt  arose  as  to  the  cause.  The  fact  that  it  was  near  the  gum 
margin  and  the  probe  could  not  be  passed  into  a  sinus  leading  to  a 
root-end  was  considered  evidence  of  abscess  secondary  to  pyorrhea. 
Evacuation  and  antisepsis  were  sufficient  to  effect  a  cure. 

In  one  case  of  pyorrhea  alevolaris  of  the  variety  under  considera- 
tion the  pocket  existed  upon  the  mesobuccal  aspect  of  a  right  lower 
third  molar.     The  second  and  first  molars  were  absent.     The  pus 
dissected  away  the  periosteum  of  the  bone  and  formed  a  large  abscess 
46 


722 


PYORRHEA  ALVEOLARIS 


over  the  entire  area  of  bone  between  the  third  molar  and  second 
bicuspid.  After  evacuation  of  the  abscess,  the  probe  was  passed 
through  it  to  the  pyorrhea  pocket  (Fig.  661).  Another  expression 
occasionally  occurs.  The  infection  travels  via  the  natural  channels 
in  the  pericementum  from  the  pyorrhea  pocket  to  a  deeper  point 
in  the  pericementum  (for  example,  to  a  point  one-quarter  inch  or 
more  below)  producing  what  is  called  a  pericemental  abscess.  The 
tissue  between  may  seem  unbroken  and  the  fistula  may  seem  like 
that  associated  with  chronic  apical  abscess.  Fig.  662  will  illustrate 
the  manner  in  which  this  may  occur.  In  a  case  of  a  pyorrhea  pocket 
on  a  lower  lateral,  transillumination  showed  a  bright  red  spot  at 
a  point  a  quarter-inch  below  the  pocket,  and  to  the  side  of  the  root. 
The  pain  was  intense,  and  only  relieved  by  opening  at  this  point 
with  a  lancet.     In  another  case  a  fistula  appeared  on  the  buccal 


Fig.  660 


Fig.  661 


Gingival  abscess  secondary  to  pyorrhea 
alveolaris :  C,  calculus  in  pyorrhea  pocket ; 
F,  fistula  leading  to  pocket  PP;  B,  bone 
on  lingual  side. 


Diagram  of  abscess  secondary  to  pyor- 
rhea alveolaris  (see  text) ;  PP,  pyorrhea 
pocket;  AC,  cavity  of  secondary  abscess; 
B,  bone. 


gum  about  one-third  inch  above  the  margin  and  between  the 
buccal  roots  of  an  upper  molar.  The  crown  was  tapped  by  a 
student  for  dead  pulp,  but  exposure  of  the  pulp  demonstrated 
its  vitality.  Exploration  showed  a  distolingual  pyorrhea  pocket 
leading  into  the  bifurcation  between  the  distobuccal  and  lingual 
roots.  From  thence  the  pericemental  abscess  discharged  buccally 
between  the  buccal  roots. 

While  dental  caries  may  occur  with  pyorrhea  alveolaris,  it  is  usual 
to  find  the  teeth  of  the  most  highly  organized  structure.  The  pulp 
tissue  is  usually  increased  in  density,  and  there  is  a  tendency  to 
the  constructive  changes,  secondary  dentin,  nodules,  etc.,  and  the 
inevitable  degenerative  changes  following  these  diseases. 

It  has  been  contended  that  these  pulps  are  responsible  in  a  measure 
for  the  pyorrhetic  condition,  and  it  is  possible  that  they  may,  by 
reflex  action,  influence  the  tissue  nutrition  of  the  pericementum  and 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     723 

gum  margin,  though  the  contrary  process  is  more  than  probable, 
as  pyorrhea  frequently  causes  a  pulp  hyperemia  which  subsides  with 
the  cure  of  the  pocket.  If  the  pulps  be  degenerated,  which  is  likely 
in  very  loose  teeth  or  deep  pockets,  their  removal  aids  the  cure  of 
the  disease  by  diverting  the  blood  they  receive  into  the  pericemental 
bloodvessels.  This  probably  counterbalances  the  effects  of  the  end- 
arteritis obliterans.     (See  Deeply  Seated  Gingivitis.) 

Fig.  662 


Pericemental  abscess  associated  with  a  pj'orrhea  pocket.     (V.  A.  Latham.) 


It  is  also  true  that  calculus  does  not  seem  to  form  as  readily  upon 
a  devitalized  tooth  as  upon  one  containing  a  vital  pulp;  it  does  form 
at  times,  however. 

Diagnosis. — The  diagnosis  is  easily  made  when  the  disease  is 
established  by  observance  of  the  phenomena  just  described.  In 
difficult  cases  with  pocket  approaching  the  apex  or  bifurcation,  a 


724  PYORRHEA  ALVEOLARIS 

skiagraph  may  be  necessary  for  accurate  determination  of  the  extent 
of  the  disease  (Fig.  655). 

Prophylaxis. — ^As  outHned  above,  the  prevention  of  pyorrhea 
alveolaris  of  the  first  class  involves  the  removal  of  the  local  and,  if 
possible,  the  systemic  causes  of  the  gingivitis,  if  any  exists,  and  the 
systematic  cleansing  of  the  teeth  at  short  intervals.  The  daily  use 
of  the  tooth-brush  and  antiseptic  powders  and  washes  by  the  patient 
is  also  important. 

D.  D.  Smith  advises,  for  this  class  of  cases,  a  thorough  cleansing 
once  a  month,  or  at  first  even  oftener.  The  cleansing  is  to  be  done 
with  an  orange-wood  point,  grasped  in  a  Jack  porte-polisher  and 
charged  with  pumice  paste,  best  made  with  hydrogen  dioxid.  The 
local  sources  of  gum  infection  are  thus  continually  removed  and  the 
gums  stimulated  by  the  mechanical  irritation  with  the  wood  point. 
Bridges  require  careful  cleansing.  (See  pp.  441  and  737  for  further 
ideas  of  prophylaxis.) 

Treatment. — The  treatment  of  well-established  pyorrhea  alveolaris 
of  the  first  class  is  to  be  considered  under  three  headings:  (1)  The 
removal  of  pus,  calculus,  and  bacterial  films;  (2)  the  prevention  of 
extreme  mobility;  (3)  the  medicinal  treatment  and  the  prophylaxis, 
or  prevention  of  a  relapse  into  the  diseased  condition. 

The  Removal  of  the  Causes. — Calculus  being  an  obvious  irri- 
tant, it  should  be  removed  from  crowns  and  all  parts  of  the  roots. 
To  prevent  infection  of  surrounding  tissues  and  to  remove  the  pus 
present  the  pockets  are  to  be  flushed  out  with  hydrogen  dioxid, 
which  may  be  done  by  means  of  a  syringe  with  fine  nozzle  after 
spraying  out  the  superficial  parts  by  means  of  an  atomizer  operated 
by  compressed  air.  The  forcible  spray  lifts  away  the  gum  margin 
and  cleanses  mechanically  as  well  as  chemically  though  not  the 
depths  of  the  pockets.  The  mouth  is  reasonably  sterilized  at  the 
same  time.  If  large  quantities  of  supragingival  calculus  exist,  it 
is  well  to  next  remove  the  gross  deposits  and  permit  the  patient  to 
use  an  astringent,  antiseptic  mouth  wash  for  a  few  days,  or  the 
operation  may  be  proceeded  with. 

Following  this,  cotton  containing  10  per  cent,  trichloracetic  acid 
may  be  packed  into  the  gum  pockets  in  order  to  superficially  con- 
stringe  the  gum  tissue,  lessen  the  hemorrhage,  and  render  more 
facile  the  removal  of  the  subgingival  calculi.  The  latter  is  accom- 
plished with  scalers  of  any  suitable  form,  working  either  with  a 
push  or  pull  cut  as  best  suits  the  case. 

Fig.  663  illustrates  the  method  ,of  guarding  against  unnecessarily 
wounding  the  soft  tissues.  If  the  calculi  be  extraordinarily  inacces- 
sible the  pockets  may  be  enlarged  by  packing  for  ten  or  fifteen  min- 


PYORRHEA   ALVEOLARIS  AS  A   MARGINAL  GINGIVITIS     725 

utes  with  cotton  tampons  saturated  with  the  10  per  cent,  trichlor- 
acetic acid,  which  also  softens  the  calculi,  or  salicylized  cotton  may 
be  left  in  the  pocket  for  a  day.  (Black.)  In  some  cases  novocain 
injections  or  applications  of  powdered  cocain  carried  into  the  pocket 
on  the  working  instruments  must  be  made  to  prevent  excessive  pain. 
After  removal  of  the  bulk  of  calculus  with  scalers  any  fine  granules 

Fig.  663 


Showing  the  manner  of  holding  an  instrument  for  detaching  calcareous  deposits 
when  using  the  pushing  motion.  The  third  finger  rests  on  the  edges  of  the  teeth,  allow- 
ing freedom  of  the  hand  to  make  rapid  and  effectual  movements  in  dislodging  the 
calculi. 


or  gummy  collections  should  be  well  rubbed  off  with  Rhein's  approx- 
imal  trimmers,  or  Smith's  pyorrhea  instruments.  After  this  medi- 
cinal applications  are  made  (see  later).  The  scaling  of  each  tooth  is 
to  be  completed  at  one  sitting,  though  more  than  one  may  generally 
be  done,  as  repeated  scalings  interfere  with  the  regenerative  process, 
and  the  pocket  is  most  accessible  at  that  time.     Hartzell  claims  that 


726 


PYORRHEA  ALVEOLARIS 


if  the  cemental  surface  be  scraped  away  to  the  depth  of  the  attach- 
ment of  the  peridental  fibers  a  source  of  infection  lying  in  these 
minute  openings  will  be  removed,  and  the  surface  will  be  left  smooth.^ 
The  lacunae  of  the  cementum  should  not  be  invaded. 


Fig.  664 


Fig.  665 


Scalers  (three  times  natural  size). 


Illustration  of  the  position  and  form  of 
incision  through  the  gum  for  exposing  the 
root  of  the  tooth  and  injured  alveolar  pro- 
cess: a,  incision.     (Black.) 


The  gum  margins  are  not  to  be  unnecessarily  wounded,  but  very 
redundant  granulations  may  be  cut  away.  In  case  the  pockets 
are  so  deep  or  have  such  form  that  the  aveolar  margins  cannot  be 
well  trimmed  without  overstretching  or  injuring  the  gingival  edges, 
Black  advises  that  gum  flaps  be  raised,  exposing  the  alveolar  margins 
(Fig.  665).  A  semicircular  incision  is  made  and  turned  back,  and 
bleeding  checked.  By  means  of  sharp  chisels  the  alveolar  borders 
are  freely  scraped,  the  pockets  are  flushed  with  hydrogen  dioxid, 
and  the  flap  secured  by  a  couple  of  stitches.  Local  anesthesia 
should  precede  this  operation.  The  same  writer  advises,  in  cases 
where  eversion  of  the  alveolar  margin  has  occurred,  that  the  process 
be  exposed  by  cuts  and  broken  down  by  three  cuts  made  with  a 
sharp  chisel  and  mallet;  the  loosened  segment  of  bone  to  be  pressed 
firmly  against  the  root.  It  is  desired  next  that  the  entire  pocket 
will  fill  with  granulation  tissue,  and  organization  of  the  granulations 
take  place,  furnishing  reattachment.  That  this  occurs  in  some  cases 
is  undoubted.  A  reproduction  of  alveolar  margins  also  occurs  in 
some  cases.  The  hope  of  good  results  lies  in  keeping  the  parts 
aseptic  after  all  foreign  deposits  and  dead  material  have  been  removed. 

In  cases  of  excessive  loss  of  the  pericementum  of  one  root  it  is  well 
to  devitalize  the  pulp,  as,  in  all  probability,  that  organ  will  have 
been  overstimulated  and  will  be  in  a  degenerative  condition,  and 
sometimes  is  actually  infected.     An  abnormal  response  to  thermal 


1  Dental  Cosmos,  1908. 


PYORRHEA  ALVEOLARIS  AS  A   MARGINAL  GINGIVITIS     727 


changes  (ordinary  cold)  may  occur  (hyperemia  or  inflammation),  or 
the  pulp  may  fail  to  respond  to  extraordinary  cold  (ethyl  chlorid), 
indicating  degeneration.  If  the  condition  be  marked  and  persistent 
after  pocket  treatment  the  pulp  should  be  removed  and  it  is  well 
to  resort  to  its  removal  at  once  when  the  pocket  approaches  the 
apex  of  the  root,  as  the  pulp  is  apt  to  be  hopelessly  affected.  It  has 
been  claimed  by  Rhein,  Smith,  and  others  that  the  nutrition  received 
by  it  will  be  diverted  into  the  pericementum,  to  the  benefit  of  the 
latter.  Clinical  experience  seems  to  confirm  this  statement.  The 
method  also  permits  the  use  of  pins  placed  in  the  root  canal  as  part 
of  an  appliance  fixing  the  teeth  in  position.  An  exposed  pocket 
in  the  bifurcation  may  be  treated  b}^  scraping  and  flowing  oxyphos- 
phate  of  copper  cement  into  it  (Figs.  666  and  667).  In  case  of 
hopeless  involvement  of  one  root  of  a  multirooted  tooth  the  root 


Fig.  666 


Fig.  667 


Pyorrhea  pocket  in  bifurcation. 


The  same  treated  by  scraping  and  filling 
with  gutta-percha  or  oxyphosphate  of  cop- 
per.    (Radiographs  by  Price.) 


may  be  amputated  if  the  remaining  roots  will  endure  the  strain 
put  upon  them.  Indeed,  the  other  roots  are  apt  to  be  firmer  if 
the  adjoining  inflammation  is  thus  removed.  The  canals  of  the 
roots  must  have  been  previously  carefully  filled. 

Rhein^  calls  attention  to  the  fact  that  collections  are  apt  to  occur 
about  the  surface  left  by  the  amputation,  and  that  postextraction 
resorption  of  the  alveolar  process  occurs.  To  obviate  this  he  suggests 
the  use  of  a  porcelain  root  to  replace  the  lost  root,  and  about  which 
the  tissues  contract  firmly  and  remain  in  a  healthy  condition.  This 
operation  Rhein  terms  "  heteroplasty  following  the  amputation  of 
natural  roots." 

Briefly  outlined  the  process  is  as  follows: 

1.  Prepare  and  fill  the  root  canals  as  far  as  the  pulp  chamber;  fill 
this  with  temporary  stopping. 


'  Dental  Cosmos,  September,  1900,  and  September,  1902 


728 


PYORRHEA  ALVEOLARIS 


2.  Amputate  the  necrosed  root  by  means  of  a  fissure  drill,  and 
remove. 

3.  Coat  the  root  with  a  film  of  paraffin  to  allow  for  shrinkage  of 
the  porcelain. 

4.  Take  an  impression  of  one-half  of  the  root  (longitudinally)  by 
embedding  in  plaster;  make  articulating  grooves  and  pour  plaster 
for  an  impression  of  the  other  half;  separate  and  remove  the  root 
from  the  plaster. 

5.  Burnish  matrix  platinum  into  each  half  of  the  impression, 
stiffen  with  porcelain,  and  reburnish.  Complete  one  side  with 
porcelain  as  in  inlay  work;  in  the  other  fuse  a  platinum  box  formed 
over  a  square  platinum  pin  (this  pin  should  be  left  in  the  box  until 
the  packing  of  the  porcelain  about  the  box  is  complete). 

6.  Flatten  the  proximating  sides  of  the  halves;  paint  with  thin, 
fresh  body;  press  together  and  fuse. 

7.  Strip  off  all  platinum  and  dress  off  all  protruding  points,  coat 
the  entire  porcelain  with  a  thin  film  of  body,  place  in  furnace  in  an 
upright  position,  and  heat  almost  but  not  quite  to  a  glaze. 

Fig.  668 


Heteroplasty  following  the  amputation  of  natural  roots.    (Rhein.) 


8.  Wash  out  socket  of  natural  root  with  antiseptics  and  remove 
temporary  stopping  from  the  crown  cavity;  try  porcelain  root  in 
place,  and  if  right  dry  everything;  fill  the  box  with  cement,  return 
the  root  to  place,  and  pass  the  pin  through  crown  cavity  and  into  the 
root  box.     Adjust  root,  leaving  a  slight  space  for  an  amalgam  joint. 

9.  Pack  the  crown  cavity  and  the  joint  with  amalgam,  and  at  a 
later  sitting  finish  the  same  (Fig.  668). 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     729 

The  Prevention  op  Excessive  Motion. — The  excessive  move- 
ment of  loosened  teeth  but  increases  the  deeply  seated  gingivitis  in 
the  remaining  tissues.  These  demand  rest.  Any  excessive  occlusion 
due  to  the  swelling  of  pericemental  tissue  may  be  compensated  for 
by  grinding  the  occluding  surfaces.  Such  excessive  occlusion  and 
motion  are  readily  detected  during  the  act  of  occluding  the  teeth 
or  by  means  of  carbon  paper.  The  fixation  of  teeth  is  a  matter  of 
mechanics,  and  the  device  used  depends  upon  the  case.  Slightly 
loosened  teeth  may  be  temporarily  splinted  with  ligatures  of  wire 
or  floss  silk.  To  prevent  the  slipping  of  these  toward  the  gum 
margin  it  has  been  suggested^  that  small  buttons  of  Harvard  or 
other  adhesive  zinc  phosphate  should  be  placed  upon  the  labial  faces 
while  under  the  rubber  dam  (Fig.  669).  The  floss  silk  may  be 
saturated  with  a  solution  of  chemically  pure  celluloid  in  acetone 

Fig.  669 


Temporary  splint  of  silk  floss  or  silver  wire  30-gauge  (one  turn  only  shown) .    Buttons 
of  zinc  phosphate.     (Rhein.) 

(155  to  500  gr.^)  to  render  it  impermeable  and  more  lasting.  The 
preparation  after  application  is  allowed  to  dry  under  the  dam  to  a 
coagulum  and  then  dismissed  for  twenty-four  hours,  when  it  may  be 
polished.  It  lasts  for  several  months.  The  wire  should  ordinarily 
be  of  brass,  as  it  is  less  likely  to  permit  caries,  and  may  be  applied 
as  a  single  strand  being  woven  in  figure-of-eight  fashion,  or  a  single 
loop  may  be  made  about  all  the  teeth  to  be  included  and  smaller 
loops  about  the  wire  at  the  interspaces,  and  these  twisted  tight  to 
effect  a  tightness  of  the  first  wire.  The  fault  in  ligatures  is  that  some 
mobility  is  always  present.  They  may  slip  toward  the  gum,  in  which 
case  a  loop  or  two  may  be  carried  over  the  occluso-interproximal 
embrasure.  For  certain  cases  Dr.  Hugh  Mitchell  has  suggested  a 
bar  of  iridioplatinum  wire  adapted  to  the  lingual  surface  of  the 
teeth  to  be  splinted,  and  soldered  to  simple  gold  bands  to  be  attached 

1  Reitz.  2  Kowarska's  paste. 


730 


PYORRHEA  ALVEOLARIS 


with  cement  to  two  of  the  teeth  adjoining  the  loose  teeth.  The 
other  teeth  are  braced  to  the  sphnt  with  fine  wire,  gold  or  platinum 
being  preferred  for  anterior  teeth. 


Fig.  671 


Fig.  672 


Diagram  showing  labial  view  of  Mitchell's 
splint,  with  two  bands  and  wiring. 


Diagram  showing  view  of  Mitchell's 
splint  with  two  bands  and  bar. 


Such  a  splint  may  be  quickly  made  and  is  very  effective,  all  slipping 
of  ligatures  being  prevented;  moreover,  the  wire  may  be  kept  away 


Fig.  673 


Fig.  675 


Five  rings  and  included  artifi-        Two  rings  and  included  artifi-        Method  of  making 
cial  tooth.     (Evans.)  cial  tooth.     (Evans.)  rings  as  in  Fig.  .538. 

from  the  necks  of  the  teeth  and  the  gums.     (Figs.  671  and  672.) 
After  a  reasonable   period  of  immobility  the  attachment  secured 


Fig.  676 


Fig.  677 


Labial  view  of  a  splint  (see  text).  Lingual  view  of  splint  shown  in  Fig.  676. 

Fig.  678 


cmnno 

Occlusal  view  of  the  splint. 

by  treatment  may  be  tested.  Very  loose  teeth  which  have  lost 
much  of  their  supporting  alveolar  process  must  be  secured  by  per- 
manent splints.     The  simplest  of  these  is  a  series  of  rings  soldered 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     731 

together,  or  its  equivalent,  shown  in  Fig.  670.  The  teeth  are  firmly 
ligated  at  their  necks  with  floss  silk.  A  wire  measure  is  taken  of 
the  entire  circumference  of  the  teeth  to  be  included,  allowance  being 
duly  made  for  burnishing.  A  piece  of  thin  platinum  or  22  k.  gold, 
No.  34  gauge  and  one-eighth  inch  w^ide,  is  cut  to  measure  and  a  lap 
joint  made  and  soldered.  The  ring  is  placed  upon  the  teeth  and 
moulded  to  their  surfaces  and  to  their  interspaces.  The  thinnest 
separating  saw  is  used  to  cut  almost  through  the  splint  on  both 
sides  at  one  interspace.  In  this  groove  a  straight  piece  of  the  plate 
is  placed  and  the  whole  withdrawn  from  the  teeth  and  the  joints 
soldered.  The  process  is  repeated  at  another  interspace  and  so  on 
until  the  piece  is  complete.  If  the  teeth  are  very  tender,  a  plaster 
impression  of  the  tips  of  the  teeth  may  be  taken  and  the  work  done 
on  a  fusible  metal  model.  If  space  be  necessary,  the  teeth  may  be 
slightly  disked  upon  their  proximal  sides.  If  such  spacing  be  not 
desirable,  the  necessary  room  can  usually  be  obtained  at  the  median 
interspace,  but  one  platinum  septum  is  placed  and  the  piece  is  to  be 
somewhat  stiffened  with  solder  at  the  indentations  representing  the 
interspaces.  To  render  the  appliance  less  conspicuous  the  entire 
lingual  side  may  be  stiffened  with  solder  and  solder  be  placed  liber- 
ally at  the  junction  of  band  and  septum  on  the  labial  side.  Nearly 
all  the  labial  portions  of  the  bands  except  the  end  ones  may  be  cut 
away,  leaving  T-buttons  at  the  labial  portions  of  the  septa  (Figs. 
676  and  678).  The  teeth  may  loosen  in  this  more  readily  than  in 
that  shown  in  Fig.  670. 

Another  valuable  device  consists  in  grinding  steps  into  the  lingual 
surface  of  an  incisor  or  cuspid.  Soft  thin  metal  is  adapted.  Three 
pins.  No.  20  guage,  are  placed,  two  incisal  straddling  the  pulp  and 
one  at  the  cervical  step.  The  whole  is  stiffened  with  solder.  Adjoin- 
ing teeth  may  be  united  by  union  of  these  plates  or  they  may  be 
used  as  anterior  abutments  of  bridges. 

It  may  also  be  used  on  centrals  and  cuspids.  For  ^^^-  ^^^ 
example,  in  a  case  of  loss  of  an  upper  cuspid  and 
lateral  the  two  centrals  were  fitted  wdth  the  tripod  step 
plates  in  Fig.  679  and  the  first  bicuspid  with  a  Carmi- 
chael,  the  pontic  teeth  then  attached.  No  pulps  were 
devitalized.  In  bicuspids  the  Carmichael  attachment  forms  a  very 
strong  abutment. 

Evans'  method  is  readily  comprehended  by  reference  to  Figs. 
673,  674,  and  675. 

These  splints  are  to  be  cemented  with  adhesive  zinc  phosphate  so 
manipulated  as  to  set  quickly.     Ames'  cements  are  excellent. 

The  foregoing  splints  are  too  conspicuous  for  use  in  some  cases 


732  PYORRHEA  A LV SOLARIS 

A  simple  device  introduced  by  Dr.  L.  C.  Bryan^  consists  of  a  pure 
gold  band  about  one-eighth  inch  wide,  nicely  bevelled  at  its  edges, 
and  adapted  about  the  necks  of  the  lower  incisor  teeth  to  be  splinted 
in  somewhat  the  same  manner  that  the  splint  illustrated  in  Fig.  670 
is  adapted.  Particular  attention  is  paid  to  the  interspaces  in  the 
endeavor  to  bring  the  labial  and  lingual  sections  together  as  nearly 
as  possible  at  that  point.  When  ready  the  piece  is  sprung  off,  the 
rubber  dam  is  applied,  zinc  phosphate  is  placed  within  the  band  and 
upon  the  necks  of  the  teeth  at  all  points,  and  the  band  is  put  in 
place  and  burnished.  Before  the  cement  has  set  gold  wire  is  to  be 
passed  around  the  interdental  portions,  tightly  twisted,  and  the 
twisted  end  cut  off  nearly  to  the  band,  and  the  remainder  bent  back 
into  the  indentation  in  the  band.  Dr.  Bryan  recommended  gold 
clamps  in  the  place  of  wire,  but  these  are  difficult  of  adaptation. 

Such  a  piece  is  to  be  placed  only  on  those  lower  incisors  about 
which  salivary  calculus  promptly  collects,  and  should  be  avoided 
in  the  mouths  of  patients  who  will  not  present  frequently  for  pro- 
phylactic service.  Confined  to  such  cases  they  do  good  service,  and 
the  cement  does  not  readily  wash  away;  indeed,  a  slight  coating  of 
calculus  seems  to  protect  the  surface  of  it  from  solution.  If  the 
calculus  be  kept  from  the  gum  this  remnant  does  no  harm. 

Several  devices  have  been  offered  which  require  the  devitalization 
of  the  pulps  and  filling  of  the  root  canals  of  the  several  teeth  to  be 
splinted. 

D.  D.  Smith^  suggests  reduction  of  the  lingual  surfaces  of  the 
teeth  and  the  fitting  to  them  of  thin  metal  backings,  which,  after 
adaptation  to  the  teeth,  are  perforated  and  pins  are  thrust  through 
for  the  root  canals.  After  soldering  each  pin  to  its  plate,  readapting 
the  latter  and  stiffening  with  solder,  an  impression  is  taken  and  the 
plates  are  united.  The  whole  piece  is  cemented  to  place  with  oxy- 
phosphate.  A  modification  for  vital  teeth  would  be  to  drill  three 
safe  pits  for  pins  for  each  plate  instead  of  the  one  central  pin  for 
the  canal,  or  to  drill  one  hole  through  the  incisal  portion  above  the 
pulp  for  each  plate.  With  this  device  one  or  more  artificial  teeth 
may  be  included  to  replace  lost  teeth  (Figs.  680  to  684).  The 
incisal  edges,  if  broad,  could  have  individual  inlays  cast  on  two 
safely  placed  pins  (Fig.  277)  and  these  soldered  together. 

Ames^  suggests  that  in  certain  cases  of  lower  incisors  the  teeth  be 
devitalized  and  amputation  be  performed  at  the  neck  of  each.  Each 
root  is  then  trimmed  and  fitted  with  a  gold  Richmond  cap  without 
pin  (Fig.  683). 

1  International  Dental  Journal,  1899. 

2  Dental  Digest,  1902.  ^  Dental  Cosmos,  1903. 


Fig.  680 


Fig.  681 


Splint  for  securing  previously  treated  lower 
anterior  teeth.     (Ames,  after  Smith.) 

Fig.  682 


Splint  for  use  in  the  case  shown  in  Fig.  681. 
Fig.  684 


Same  as  Fig.  681.    Splint  in  position. 
Fig.  685 


Upper  teeth  prepared  for  splint. 
(Ames.) 

Fig.  683 


Root  with  cap  fitted.     (Ames.) 
Fig.  686 


Tooth  with  Richmond  cap.     (Ames.)      Splint  for  lower  incisors.     (See  text.)    (Ames.) 


734 


PYORRHEA  A LV SOLARIS 


Each  natural  crown  is  slightly  trimmed  and  fitted  with  a  gold 
Richmond  cap  with  a  pin  (Fig.  685).  These  two  caps  are  united 
with  wax,  carried  to  the  mouth,  and  adjusted  in  position.  Each  is 
then  carefully  removed,  the  natural  crown  laid  aside  (in  water), 
and  the  gold  sections  invested  and  soldered  together.  The  individual 
parts  are  readjusted  in  the  mouth,  an  impression  taken,  an  invest- 


FiG.  687 


Splint  for  lower  incisors.      (See  text.)      (Ames.) 
Fig.  688 


Splint  and  double  saddle  bridge  combined.    ] 


V.     (Ames.) 


ment  made,  and  all  soldered  together.  The  natural  crowns  are  then 
fastened  in  their  prepared  sockets  with  cement,  and  the  piece  is 
cemented  to  place.  Pins  may  be  placed  in  the  roots  if  desired 
(Fig.  686). 

If  desired  the  piece  may  be  further  attached  to  the  adjoining 
teeth  by  means  of  the  lingual  plate  and  pin  (Fig.  687).     The  Ames 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     735 

device  would  be  useful  in  cases  in  which  approximal  cervical  caries 
exists. 

It  may  be  stated  that  three  or  four  teeth  fairly  loose  individually, 
when  united  together  may,  as  a  whole,  be  quite  firm. 

Ames  claims  that  the  extension  bridge  shown  in  Figs.  688,  689, 
and  690  lasted  for  years  and  was  in  as  good  condition  then  as  at  the 
beginning.  Fig.  688  gives  the  anterior  view.  Fig.  689  that  of  the 
right  side,  and  Fig.  690  that  of  the  left  side. 


Fig.  689 


Fig.  690 


Right  side  of  extension  brie 
Fig.  688. 


in  Left  side  of  extension  bridge  shown  in 

Fig.  688. 


Rhein  offers  the  following:  After  pulp  removal  and  root  filling  a 
transverse  groove  is  cut  in  the  lingual  side  of  the  central  or  loose 
teeth  and  a  half-groove  upon  the  mesiolingual  aspect  of  the  pier 
teeth.  A  staple  is  formed  of  triangular  iridioplatinum  wire  to  fit 
into  the  root  canals  of  the  pier  teeth.  To  this  is  soldered  a  pin  for 
each  of  the  central  teeth.  The  face  of  the  wire  should  approximately 
fit  the  bottom  of  the  groove  (Fig.  691).  Rhein  suggests  the  following 
method  of  attachment:  (1)  Fill  the  root  with  a  paper  point,  place 
cement  over  that,  and  fill  the  cervical  margin  of  the  cavity  and  its 
floor  with  gold;  (2)  drill  through  the  gold  to  the  paper  point,  remove 
it,  and  refit  the  retaining  appliance;  when  ready  set  with  zinc  phos- 
phate, avoiding  excess;  (3)  when  this  is  set  cut  away  to  the  gold 
and  complete  the  gold  fillings. 

A  less  elegant  but  still  practical  method  would  be  to  cover  the 
pins  with  a  good,  color-keeping  amalgam  pressed  into  the  excess  of 
cement  before  it  has  set.  The  margins  are  then  to  be  freed  of  cement 
and  the  operation  completed  with  amalgam,  which  later  should  be 
polished.  In  undecayed  teeth  this  has  no  advantage  over  the  method 
shown  in  Fig.  680;  nor  in  decayed  teeth  over  that  in  Fig.  685. 


736  PYORRHEA  ALVEOLARIS 

Smith's,  Rhein's,  and  Ames'  devices  permit  the  use  of  an  artificial 
tooth  if  necessary.  The  same  may  be  said  for  the  device  which 
consists  of  a  series  of  gold  rings  (Evans') . 

For  the  molars  and  bicuspids  Rhein's  device  is  transferred  to  the 
occlusal  surface  (Fig.  692). 

Short  metal  caps  made  for  the  incisal  tips  of  lower  incisor  teeth 
adjoining  a  space  will  successfully  hold  a  bridge  tooth.  The  device 
is,  however,  rather  conspicuous.  Well  anchored  gold  inlays  joined 
by  solder  or  cast  together,  or  a  staple  in  two  or  more  roots  of 
different  teeth  about  which  staple  fillings  are  later  built  may  be 
useful.     Carmichael  attachments  will  serve  for  some  teeth. 

For  the  molar  and  bicuspid  teeth  it  seems  good  practice  to  adapt 
short  crowns  to  the  teeth  trimmed  only  to  the  fullest  point  of  con- 
tour, and  unite  these  with  solder.  Occasionally  the  bands  may  be 
slit  occlusally  and  adapted  closely  without  covering  the  cusps.  A 
sort  of  bridge  is  thus  made  which  causes  the  teeth  to  be  firm  even 
if  all  are  originally  loose  (Fig.  693).  It  is  mainly  this  factor  which 
renders  bridge-work  useful  in  pyorrhea  alveolaris  upon  isolated 
teeth.  If  the  necks  of  such  teeth  are  hypersensitive,  silver  nitrate  may 
be  used.  This  device  is  especially  useful  when  teeth  are  inclined. 
As  an  example,  an  upper  third  and  second  molar  were  fitted  with 
short  crowns,  a  first  bicuspid  with  a  Carmichael  and  a  pontic 
bicuspid  used.     The  united  held  the  three  loose  teeth  very  firmly. 

The  use  of  united  barrel  crowns  reaching  the  gum  margins  is  at 
times  useful,  but  the  configuration  of  exposed  roots  may  render  this 
impossible  in  some  cases. 

By  the  use  of  pure  gold  crowns,  which  may  be  stiffened  occlusally 
with  solder  to  gain  strength,  better  adaptation  at  cervical  portions 
may  be  obtained  by  hand  burnishing  after  cementation  of  the  piece. 

All  appliances  cemented  to  the  teeth  and  having  a  free  margin  are 
subject  in  some  degree  to  a  solution  of  the  cement.  These  cases 
should  be  seen  frequently  in  any  event  for  prophylactic  purposes, 
when  the  condition  of  the  appliance  may  be  noted. 

Extraction  and  bridge-work  may  be  at  once  resorted  to  in  some 
of  the  aggravated  cases,  though  if  the  appliance  be  mechanically 
constructed  teeth  which  may  be  extracted  with  the  fingers  may  be 
firmly  held  in  splints  for  years.  While  this  is  a  fact,  good  judgment 
may  demand  the  early  removal  of  such  teeth  before  an  appliance  is 
constructed. 

E.  Ewing  Roach^  has  suggested  that  in  case  of  loose  incisors  drill 
holes  may  be  made  from  mesial  to  distal  or  the  reverse,  and  a  plati- 

1  Dental  Cosmos,  1908,  p.  65. 


PYORRHEA  ALV SOLARIS  AS  A  MARGINAL  GINGIVITIS     737 


num  wire,  18  or  20  gauge,  be  cemented  through  the  several  teeth. 
The  cases  must,  of  course,  be  selected. 

If  desired  the  bridge  may  be  made  so  as  to  mount  the  natural  teeth 
after  their  extraction,  by  constructing  sockets  of  gold  for  the  recep- 


FiG.  691 


Fig.  693 


Permanent  splint  for  cases  of  pyorrhea  alveo- 
laris  on  molars  and  bicuspids. 


Permanent  splint  for  cases  of  pyorrhea  alveo- 
laris  in  upper  or  lower  incisors.     (Rhein.) 

Fig.  692 

tion  of  the  necks  of  the  teeth 
somewhat  after  the  manner 
employed  in  the  Ames  method. 
The  sockets  are  then  soldered 
to  each  other  and  to  the 
bridge  piers,  after  which  the 
teeth  are  attached. 

These  sockets  are  to  be 
made  deep  at  first,  and  it  is 
well  to  attach  the  teeth  with  gutta-percha  in  order  that  the  row  of 
sockets  or  a  new  row  may  be  lowered  to  fit  the  gum  if  desirable.  This 
will  require  the  raising  of  the  teeth  to  the  occlusal  level.  Occasionally 
the  use  of  the  overarch  bar  is  demanded  to  prevent  the  overuse  of  the 
teeth  acting  as  piers  for  bridge-work.  The  lateral  support  of  teeth  by 
plates  is  occasionally  of  use  in  pyorrhea,  but  the  question  requires 
careful  consideration.  (See  p.  664.)  The  prevention  of  mobility  in 
advanced  cases  may  be  at  times  an  impossibility.  In  such  cases 
extraction,  and  the  use  of  artificial  teeth,  is  probably  better  judg- 
ment than  the  retention  of  the  teeth  until  extracted  one  by  one.  In 
all  cases  the  element  of  overuse  must  be  considered  and  anything 
possible  done  to  prevent  it.  (Read  carefully  page  661.)  Also 
anything  that  may  induce  gingivitis  as  a  riding  plate  festoon  must, 
if  possible,  be  avoided. 

The  Medicinal  Treatment  and  Prophylaxis. — Simple  cases  often 
heal  spontaneously  after  thorough  work  and  antisepsis.  If  aseptic 
a  clot  drawn  after  the  irrigation  of  the  pocket  with  hydrogen  dioxid 
is  often  useful.  Some  operators  depend  upon  blood  flow.  In  order 
to  control  the  patient  and  watch  the  case,  any  pocket  existing  after 
a  week  should  be  washed  out  with  hydrogen  dioxid  and  then  filled 
with  balsam  of  Peru  which  can  be  kept  ready  at  hand  in  a  Safety 
Sub.  Q  syringe.     This  substance  is  a  mild  antiseptic  stimulant  of  a 

47 


738  PYORRHEA  ALVEOLARIS 

viscidity  sufficient  to  fill  the  pockets  even  though  wet,  if  the  needle 
is  inserted  to  the  bottom.     Thereafter  it  should  be  used  twice  a  week. 

If  the  case  refuse  to  heal  there  may  be  calculus  overlooked  upon 
the  roots.  An  acid  is  used  to  soften  this  if  not  removable  by  instru- 
ments. Head  recommends  the  use  in  the  pockets  on  each  fourth 
day  of  ammonium  bifluorid^  as  a  solvent  of  calculus  and  tissue 
stimulant.  It  does  not  dissolve  enamel  or  cementum.  The  tissues 
are  to  be  protected  against  burns  from  any  overflow,  which  must  be 
removed.  It  produces  no  harm  within  two  minutes.  It  is  to  be 
injected  with  a  rubber  syringe  with  a  platinum  point  (Dunn  syringe). 

Lactic  acid  full  strength  (Younger),  trichloracetic  acid,  25  per 
cent,  strength  (Kirk) ;  sulphuric  acid,  25  per  cent,  strength  (Truman) 
are  all  solvent  for  tartar,  and  stimulant  germicides  if  infection  con- 
tinues the  ulceration. 

As  an  astringent  antiseptic  zinc  chlorid  deliquesced,  or  sulpho- 
carbolate  of  zinc  in  10  per  cent,  solution,  or  zinc  iodid  in  10  per  cent, 
solution,  or  copper  sulphate,  10  per  cent.,  are  all  useful. 

As  an  astringent  lotion,  zinc  chlorid,  gr.  x  to  each  fluidounce  of 
aquse  rosse,  aquae  gaultherise,  aquse  menthi  piperitse,  etc.,  may  be 
applied  by  the  patient  daily  on  a  cotton  swab  made  by  rolling  cotton 
on  the  end  of  a  tooth  pick.  It  may  be  diluted  to  an  agreeable  astring- 
ence  for  a  mouth  wash  (or  two-minute  bath),  or  tincture  of  iodin 
may  be  applied  every  other  day,  or  iodoglycerol  (see  p.  680)  may 
be  painted  upon  the  gums. 

Gentle  massage  of  the  gums  by  means  of  the  finger-tips  stimulates 
the  tissues  and  squeezes  out  secretions.  If  common  table  salt  be 
used  in  conjunction  the  stimulant  antiseptic  effect  is  obtained. 
Powdered  sulphur  is  recommended  by  Gordon  White  instead. 

The  use  of  a  strong  stream  of  water  from  a  syringe  is  recommended 
by  Black  to  wash  away  the  agglutinin  collected. 

Dr.  A.  B.  Harrow^er  has  suggested  the  following  formula  for  a 
powder  which  has  in  his  own  and  my  hands  given  good  results  as  an 
astringent  antiseptic: 

I^ — Magnesium  carbonate .      lb.  j 

Cream  of  tartar lb.  iss 

Red  cinchona  bark §ij 

Calcined  alum §j 

Oil  peppermint >      .       .       .    f5v 

Oil  cinnamon f  Biij 

Oil  rose  geranium f  5j 

All  ingredients  to  be  finely  powdered.  The  oils  are  to  be  added  to  the  magnesium 
before  thorough  mixing  of  the  powders.    The  whole  is  to  be  sifted  through  silk. 

Saccharin  may  be  added  to  the  above  as  a  sweetening  agent.  The  powder  when 
wet  is  almost  neutral,  and  should  do  no  harm  in  its  limited  use  as  a  therapeutic  agent. 

1  "Tartar  Solvent,"  or  "Tartasol,"  is  made  by  neutralizing  hydrofluoric  acid  with 
ammonium  carbonate,  filtering,  evaporating  to  half  the  bulk,  adding  again  an  equal 
bulk  of  hydrofluoric  acid,  and  again  evaporating  to  one-half  bulk  (at  90°  to  105°  F.). 
(Items  of  Interest,  1909,  p.  175.) 


PYORRHEA   ALVEOLARIS  AS  A   MARGINAL  GINGIVITIS     739 

Black  has  recommended  the  use  of  the  1-2-3  mixture,  or  phenol- 
camphor,  to  be  put  into  the  pockets  every  three  days,  and  a  few 
drops  to  be  used  on  the  tooth  brush. 

I^ — Oil  of  cinnamon 1  part 

Carbolic  acid 2  parts 

Oil  of  gaultheria 3  parts 

I^ — Gum  camphor, 

Crystal  carbolic  acid aa     q.s. 

Mix  in  a  mortar  to  an  oily  fluid. 

Barrett  injects  as  an  amebacide  a  one-half  of  1  per  cent,  solution 
of  emetin  hydrochlorid  in  normal  saline  solution  into  the  tissue  at 
the  bottom  of  a  pocket  and  fills  the  pocket  with  the  solution,  repeat- 
ing this  on  several  consecutive  days  (see  p.  714). 

Regeneration  in  the  pockets  should  not  be  disturbed,  so  that 
unless  the  pus  flow  be  active  one  should  wait  until  sufficient  time  has 
been  afforded  (about  a  week  or  ten  days)  for  granulations  to  form. 
If  pus  be  then  detected  the  pocket  should  be  again  treated  thoroughly. 
Good  results  are  obtained  from  the  use  of  an  astringent  antiseptic 
wash  used  in  forcible  spray  from  an  atomizer  or  introduced  by  means 
of  a  syringe.  This  should  be  done  daily  by  the  patient.  Stagnant 
fluids  in  the  pockets  are  washed  out  and  replaced  by  the  antiseptic, 
thus  inhibiting  the  bacterial  growth  in  the  pockets  and  the  mouth. 

The  teeth  should  be  cleansed  after  meals  to  prevent  media  for 
infection  lodging  about  the  interstices,  after  which  the  antiseptic 
spray  wdll  aid  in  inhibiting  bacteria.  If  the  case  still  refuse  to  heal 
Beck's  bismuth  paste  may  be  used. 

I^ — Bismuth  subnitrate 30  parts 

White  wax 5  parts 

Paraffin 5  parts 

Vasehn 60  parts 

Mix  while  boiling. 

It  is  injected  from  a  syringe  kept  for  the  purpose. 

Good  results  from  the  application  of  the  x-rays  and  high-frequency 
currents  have  been  claimed  by  Parker,^  Price,  Guy,  Satterlee,  Tousey, 
and  others 

Raper  claims  that  the  otherwise  incurable  cases  are  not  benefited. 

The  local  treatment  outlined  must  first  be  given  and  the  a;-rays 
and  high-frequency  currents  used  as  an  adjunct. 

Tousey  recommends  an  a:-ray  tube  made  of  lead  glass  except  for 
a  single  window  of  ordinary  glass,  through  which  the  rays  pass  in 
one  direction  only,  and  thus  both  patient  and  operator  are  protected 
from  the  unintentional  action  of  the  rays. 

1  Dental  Cosmos,  December,  1903. 


740  PYORRHEA  ALVEOLARIS 

Applications  of  a  minute  or  two  have  beneficial  effect.  The  high- 
frequency  currents  are  applied  by  small  vacuum  tubes  or  electrodes 
directly  to  the  gums.  They  contain  and  emit  violet  and  ultra-violet 
rays,  which  not  only  stimulate  the  part  through  the  electricity,  but 
also  produce  ozone  upon  the  gum  surface  and  carry  it  in  and  also 
produce  ozone  in  the  tissue  by  electrolysis. 

The  use  of  vaccines  seems  indicated  in  the  more  serious  cases 
not  yielding  to  local  treatment,  the  predominant  bacteria  being 
employed  in  the  autogenous  vaccines.  In  past  treatments  these 
vaccines  have  only  aided  in  resistance  to  the  pyogenic  infections, 
and  some  report  good  results  from  their  use.  A.  H.  Merritt^  claims 
that  after  exhaustive  trial  he  has  found  them  of  no  greater  use  than 
local  treatment.  As  yet  no  one  knows  the  exact  cause  of  pyorrhea, 
so  it  can  not  be  said  that  the  treatment  has  proceeded  upon  scien- 
tific lines. 

McGehee^  claims  about  50  per  cent,  of  cases  improved  markedly 
through  the  use  of  the  Van  Cott  stock  vaccines,  of  which  each  bulb 
contains  in  1.0  c.c:  Streptococcus,  50,000,000;  bacilli  coli  communis, 
100,000,000;  pneumococcus,  100,000,000;  staphylococcus  (combined 
aureus,  albus,  and  citreus),  500,000,000,  killed  and  in  sterile  solution. 

He  claimed  his  best  results  were  obtained  by  beginning  with  one- 
fourth  of  the  bulb  content,  0.25  c.c,  injecting  at  four-day  intervals, 
later  increasing  to  0.50  c.c,  and  up  to  six,  seven,  or  eight  injections 
all  told.  An  effort  has  been  made  to  utilize  the  opsonic  index  in 
the  diagnosis  of  pyorrhea  alveolaris  and  its  treatment  by  means  of 
vaccines  prepared  from  the  variety  of  germ  found  to  be  the  probable 
infection.  It  may  be  stated  that  the  effort  is  to  raise  the  opsonic 
index,  or,  in  other  words,  the  property  of  the  blood  serum  which 
assists  or  promotes  phagocytosis,  so  that  the  infection  may  be  killed 
out.  That  is,  the  resistive  force  of  the  patient  to  the  particular 
infection  is  raised.    (See  p.  63.) 

Good  results  have  been  obtained  in  some  cases  by  extraction  and 
replantation,  after  root  preparation  and  sterilization  of  the  tooth  and 
alveolus.     The  alveolus  may  have  to  be  deepened. 

If  the  interstitial  gingivitis  underlying  the  case  be  of  systemic 
origin — i.  e.,  due  to  auto-intoxication  from  any  disease,  the  alimen- 
tary canal,  the  pyorrhea  itself,  or  to  drug  action — these  should  have 
attention.  The  systemic  disease  should,  if  possible,  be  cured  by 
correct  medical  attention.  Pyorrhea  patients  are  of  the  hyperacid 
type  (Michaels),  and  treatment  should  be  directed  toward  elimina- 

1  Remarks  before  Pennsylvania  State  Dental  Society,  1914.  See  Dental  Cosmos  for 
1914. 

2  Dental  Cosmos,  September,  1912. 


PYORRHEA  ALVEOLARIS  AS  A  MARGINAL  GINGIVITIS     741 

tion  of  waste  products  and  the  reduction  of  hyperacidity  by  the  use 
of  alkahne  remedies.  The  bowels  should  be  kept  active  and  the  skin 
pores  open.  Brisk  exercise  in  the  open  air,  if  not  specifically  contra- 
indicated  by  organic  disease,  is  valuable  in  both  directions.  Warm 
baths  followed  by  cold  douches  and  vigorous  rubbing  stimulate  the 
skin.  Turkish  baths  followed  by  massage  directed  to  stimulation 
of  the  eliminating  organs  are  valuable  unless  contra-indicated.  Free 
drinking  of  pure  water  is  necessary  to  the  successful  elimination  of 
the  waste  products  of  the  body.  The  water  entering  the  blood 
increases  the  blood  pressure  and  flushes  the  tissues  and  the  kidneys, 
dissolving  waste  products.  Water  should  be  freely  taken  between 
or  before  meals  in  order  that  digestion  be  not  interfered  with,  and 
if  medicated  with  salts  of  lithium  the  alkalinizing  effect  and  solvent 
action  of  lithium  upon  urates  are  obtained.  Patients  exhibiting  an 
aversion  to  water  drinking  are  more  apt  to  take  it  when  medicated 
than  as  a  physiological  necessity.     (See  also  pp.  105  and  689.) 

The  prophylaxis  of  pyorrhea  alveolaris  is  all  important,  especially 
in  the  cases  in  which  chronic  disease  or  malnutrition  may  not  be 
readily  overcome  owing  to  confirmed  habit  of  life  or  advanced  stage 
of  disease.  The  local  conditions  existing  even  after  a  cure  of  pyorrhea 
are  such  as  to  invite  reinfection,  and  the  establishment  of  microbic 
plaques,  which  frequent  cleansing  of  the  teeth  will  remove.  The 
system  of  monthly  or,  if  necessary,  more  frequent  prophylaxis 
advocated  by  D.  D.  Smith  should  be  practised.  Its  good  results 
are  particularly  manifest  in  this  class  of  cases.  Also  the  use  of  the 
prophylactic  stick  by  the  patient  twice  a  week  and  the  careful  and 
proper  use  of  floss  is  very  beneficial.  The  patient  performs  these 
manipulations  with  difficulty,  and  is  apt  to  backslide.     (See  p.  442.) 

Recurrence  of  the  condition  is  probable  if  the  oral  prophylaxis  or 
systemic  treatment  be  neglected.  The  simpler  cases  yield  quite 
readily;  the  advanced  ones,  in  which  much  of  the  alveolar  process 
is  lost,  and  especially  when  the  gums  are  flabby  and  admit  food  to 
the  pockets,  tax  the  patience  of  operator  and  patient  alike,  and  are 
apt  to  end,  sooner  or  later,  in  loss  of  the  teeth  affected. 

This  fact,  however,  should  not  prevent  the  retention  of  these 
teeth  by  every  means  at  command  during  the  period  for  which 
they  may  be  made  useful.  If,  however,  any  tooth  prove  an  incurable 
source  of  pus  formation,  or  from  the  first  be  likely  so  to  do,  it  should 
be  removed,  otherwise  the  remaining  teeth,  and  possibly  the  patient's 
blood,  are  continuously  infected.  The  mouth  will  often  be  markedly 
benefited  at  the  start  if  a  few  bad  teeth  are  removed,  and  bridge 
work  be  inserted,  to  supply  their  places,  thus  removing  the  indi- 
vidual strain  and  splinting  the  remaining  teeth. 


742  PYORRHEA  ALVEOLARIS 


SYSTEMIC  EFFECTS  OF  PYORRHEA  ALVEOLARIS. 

It  has  been  abundantly  shown  by  Hunter  and  others  that  the  pus 
of  pyorrhea  and  other  intense  oral  sepsis  is  a  source  of  systemic 
infection,  producing  effects  ranging  from  gastritis  to  actual  septic 
infection.  The  importance  of  this  fact  is  not  to  be  lost  sight  of,  and 
patients  are  to  be  informed  of  the  dangers  of  constant  pus  formation, 
as  well  as  of  the  presence  of  other  forms  of  sepsis  about  the  mouth 
and  teeth. 

R.  D.  Watkins,  M.D.,  has  examined  the  blood  of  pyorrhetic 
patients,  and  has  found  a  mild  condition  of  septic  blood  similar  to 
but  less  than  found  in  puerperal  fever  and  advanced  carcinoma  and 
in  other  infective  conditions.^ 

Goadby^  reports  the  cure  of  a  case  of  profound  muscular  weakness, 
mental  depression,  and  insomnia  after  unavailing  general  medical 
treatment  for  neurasthenia,  as  following  the  extraction  of  teeth 
affected  by  pyorrhea.  VaneP  cites  a  case  of  chronic  septicemia  with 
symptoms  of  pallor  and  asthenia,  and  ecchymotic  patches  (see  p. 
119)  on  the  legs,  associated  with  pus  formation  about  the  roots  of 
teeth.  The  symptoms  disappeared  in  a  few  weeks  after  the  oral 
treatment. 

Hunter  and  Leith^  have  described  cases  of  subacute  and  chronic 
catarrh  of  the  stomach  and  phlegmonous  gastritis  due  to  the  ordinary 
pyogenic  cocci,  such  as  are  found  in  the  mouth,  and  which  the  gastric 
juice  of  the  stomach  of  the  particular  individual  at  least  was  not 
competent  to  kill.  Considering  the  fact  that  an  oral  subacute 
catarrhal  condition  is  established  in  pyorrhea,  the  local  transfer  of 
the  infection  is  not  surprising.  Park^  believes  many  cases  of  appen- 
dicitis to  be  due  to  oral  infection. 

Kirk  adds  to  this  list  pernicious  anemia,  bronchopneumonia, 
malignant  endocarditis,  pyemic  lymphadenitis,  etc.,  as  possibilities 
of  secondary  infection  or  extension  by  natural  contiguous  channels. 

HartzelP  claims  that  three  deaths  from  septic  endocarditis  were 
traceable  to  violent  pyorrhea. 

Skinner  instances  a  case  of  intestinal  infection,  accompanied  by 
nervousness  and  weakness,  with  confinement  to  bed  for  three  months, 
as  rapidly  and  steadily  improving  after  the  treatment  of  a  pyorrhea 
with  profuse  suppuration.     Rheumatism  and  even  arthritis  defor- 

1  Items  of  Interest,  1904.  ^  International  Dental  Journal,  July,  1902. 

3  Dental  Cosmos,  1908,  p.  192. 

*  Transactions  Odontological  Society  of  Great  Britain,  International  Dental  Journal, 
1899. 

5  Surgery  by  American  Authors.  ^  Dental  Cosmos,  1908,  p.  240. 


PYORRHEA  ALVEOLARIS  743 

mans  have  been  claimed  as  associated  with  pyorrhea,  the  infection 
being  absorbed  by  the  lymphatics  associated  with  the  teeth.  The 
bacteriology  of  this  relation  is  now  being  investigated.  The  organ- 
ism most  often  oflFending  is  the  Streptococcus  viridans,  which  may 
be  isolated  from  the  blood  of  the  patients  suffering  from  a  general 
infection  due  to  a  local  focus  of  infection,  whether  this  be  in  the 
appendix,  tonsil,  or  a  dental  abscess  or  pyorrhea  pocket.  It  growls 
upon  blood  agar  with  a  green  color  in  its  colonies.  If  the  same 
bacterins  can  be  isolated  from  the  blood  and  the  focus  and  the 
condition  clear  up  upon  removal  of  the  latter,  the  relation  is 
absolute.     (See  p.  631  and  Index  under  Bacteria.) 

PYORRHEA  ALVEOLARIS  NOT  DEPENDENT  UPON  CALCULUS 

FORMATION. 

A  form  of  pyorrhea  occurs  in  which  calculus  does  not  seem  to  be 
the  exciting  or  contributory  cause.  It  seems  rather  to  be  due  to 
infection  localized  in  soft  bacterial  collections  in  localities  protected 
from  ordinary  friction. 

Sometimes  no  perceptible  calculus  can  be  found  upon  the  roots, 
but  a  soft  gummy  collection  may  be  noted.  The  forms  of  the  necks 
of  the  teeth  readily  permit  bacterial  collections  and  the  infection 
causes  a  bright  red  marginal  gingivitis.  A  pocket  forms  and  the 
infection  becomes  deep.  The  gum  tissue  is  sometimes  destroyed 
between  two  teeth.  There  is  often  evidence  of  infection  of  other 
gum  margins  with  the  bright  red  color.  In  another  form  the  gum 
margins  are  separated  from  the  teeth.  Pockets  are  formed  which 
collect  food.  There  is  not  much  pus  apparent,  but  there  is  a  pig- 
stye  odor  of  putrefaction.  The  marginal  bone  is  lost.  In  another 
form  a  deep  pocket  forms  and  necrotic  bone  may  be  found. 

The  advance  of  the  disease  is  sometimes  rapid  and  sometimes  not. 
Sometimes  a  lateral  abscess  is  associated  with  it.  The  diagnosis  is 
that  of  pyorrhea  alveolaris  of  aggravated  type,  and  probably  special 
infection,  and  its  progress,  symptoms,  and  treatment  are  practically 
the  same  as  in  the  first  class. 

The  advance  of  the  case  may  be  very  slow  and  limited  to  the 
teeth  originally  involved.    The  following  is  an  example : 

Miss  H.,  aged  twenty-five  years,  presented  with  well-established 
pockets,  extending  one-half  inch  tow^ard  the  apex,  upon  the  mesial 
aspect  of  the  root  of  the  right  upper  central  incisor  and  distal  and 
distobuccal  aspect  of  the  right  upper  lateral  incisor.  There  was  a 
history  of  traumatism  due  to  violent  and  persistent  wedging  with 
rubber  at  about  the  age  of  sixteen.    The  case  was  then  of  several 


744  PYORRHEA  ALVEOLARIS 

years'  standing,  and  the  two  teeth  elongated  about  one-eighth  inch 
beyond  their  fellows  (Fig.  694).  There  was  no  subgingival  calculus. 
The  pockets  were  treated  wdth  some  benefit,  and  the  teeth  shortened 
for  the  cosmetic  effect,  but  the  patient  left  the  city  suddenly  before 

Fig.  694 


Pyorrhea  alveolaris  without  calculus.  Pockets  as  shown.  Teeth  were  one-sixteenth 
inch  longer,  but  have  been  shortened.  Practically  no  calculus  and  but  slight  flow  of 
thick,  creamy  pus.     Gum  prominent  over  affected  teeth.    Condition  in  1904. 

recovery,  and  was  not  seen  again  for  three  years.  At  this  second 
visit  it  was  found  that  the  pockets  were  nearly  the  same  as  at  first, 
and  no  other  teeth  had  become  involved.  Nor  had  the  teeth  further 
elongated. 

During  the  four  years  from  1904  to  1908,  elongation  and  grinding 
reduced  nearly  all  the  crown  of  the  lateral,  which  had  one-quarter 
inch  of  its  root  cervix  exposed.  Coincidently  with  the  exfoliation  the 
pockets  disappeared  as  though  by  a  drawing  up  of  the  bottom.  The 
two  teeth  were  finally  lost.  The  consideration  of  this  form  of 
pyorrhea  should  be  that  it  is  specially  virulent. 


CHAPTER  XXV. 

PERICEMENTAL  ABSCESS. 

In  comparatively  rare  cases  there  begins  in  the  lateral  aspect  of  a 
pericementum  a  swelling  which  finally  discharges  its  contents  either 
at  the  gum  margin  or  directly  through  the  gum  tissue. 

The  pulp  of  the  tooth  may  be  perfectly  vital  and  the  attachment  at 
the  gum  margin  at  first  at  least  practically  unbroken.  A  deposit  of 
calculus  may  or  may  not  be  formed  in  the  area,  and  the  discharge  may 
consist  of  a  glairy  fluid  or  of  purulent  matter.  Cases  of  this  disease 
have  been  noted  and  described  by  Darby  (1874),  W.  E.  Walker 
(1895),  Talboti  (1896),  D.  D.  Smith  (1897),  and  Kirk  (1898).  Black 
claims  that  he  has  never  found  such  a  condition  without  local  injury. 

Forms  of  Pericemental  Abscess. — There  are  four  forms  of  perice- 
mental abscess  as  described  and  seen : 

1.  An  ordinary  pyorrhea  begins  at  the  gum  margin  and  extends 
into  the  alveolus  at  the  expense  of  the  pericementum.  The  bacteria 
find  their  way  to  the  bottom  of  the  pocket  or  into  the  tissue  at  its 
side.  They  develop  in  the  said  location  and  the  pus  burrows  into 
the  lateral  gingival  tissue,  causes  swelling  and  pointing,  and  dis- 
charges at  the  lateral  gingival  aspect  or  analogous  situation.  (See 
p.  721.)  This  is  not  always  opposite  the  gum  orifice  of  the  pocket. 
(See  Figs.  660  and  661.)  In  one  case  a  fistula  was  found  at  the  buccal 
aspect  of  the  gum  opposite  a  point  midway  between  the  buccal  roots 
of  an  upper  molar  at  the  middle  third  of  the  roots.  The  pulp  was 
exposed  and  vital,  having  been  drilled  to  on  the  supposition  of  its 
death.  A  gum  pocket  was  found  at  the  distolingual  aspect  of  the 
lingual  root  and  the  pus  had  burrowed  into  the  bifurcation  between 
the  lingual  and  distobuccal  root,  and  discharged  as  stated,  remain- 
ing as  a  chronic  abscess.  There  is  a  simple  acute  condition  of  this 
kind  of  origin  seen  occasionally.  A  swelling  of  the  gum  margin 
occurs  and  pointing  occurs,  lancing  usually  demonstrates  pus  present 
and  effects  a  cure.  The  infection  has  entered  the  gingival  space, 
travelled  into  the  tissue  and  developed  what  may  be  termed  a  true 
marginal  gingival  abscess. 

1  International  Dental  Journal,  1896. 

(745) 


746  PERICEMENTAL  ABSCESS 

2.  There  is  a  pyorrhetic  condition  at  the  gum  margin;  later  an 
abscess  develops  on  the  lateral  aspect  at  a  point  a  little  higher  up 
toward  the  apex,  usually  at  the  gingival  third.  There  may  be  no 
detectable  connection  between  the  two,  but  probably  a  deeper 
infection  has  occurred,  the  avenue  being  along  the  connective  tissue 
spaces,  the  bloodvessels  or  the  glands  of  Black.  In  one  case  of  this 
sort  the  fistula  was  formed  over  the  highest  point  of  the  middle 
third  of  the  root  of  a  cuspid  retained  for  plate  work.  The  gum 
margin  was  flabby,  but  not  markedly  pyorrhetic.  There  was  firm 
tissue  at  the  bottom  of  the  space  on  all  sides.  The  pulp  was  vital. 
Examination  showed  a  small  calculus  on  the  root  surface  below  the 
fistula.  The  abscess  tract  was  limited.  Sometimes  it  is  of  greater 
extent.     Fig.  662  will  illustrate  how  this  occurs. 

3.  An  acute  swelling  occurs  over  a  root,  the  gum  margin  is  un- 
broken, a  discharge  of  glairy  or  purulent  material  occurs,  and  a 
calculus  or  none  may  be  found.  In  this  connection  Fig.  297  shows 
that  a  calculus  may  exist  as  a  primary  cause  of  the  pericemental 
abscess.  As  calculi  of  gouty  (sodium  bi-urate)  or  other  origin  occur 
in  other  parts  of  the  body  and  in  the  pulp,  there  is  no  valid  reason 
why  one  should  not  occur  in  the  pericementum  or  upon  the  root 
under  it  if  some  sluggish  condition  of  the  circulation  renders  the 
tissues  into  a  degenerative  state  favoring  it.  (See  p.  103.)  The  peri- 
cementum contains  white  fibrous  tissue  which  is  particularly  prone 
to  such  deposits. 

Whether  such  a  deposit  occurred  primarily  in  the  case  of  the  cuspid 
described  under  Class  2  and  infection  followed,  or  whether  the  infec- 
tion and  pus  came  first  and  the  calculus  followed  is  not  quite  clear. 
In  two  distinct  cases,  with  healthy  gum  margins,  the  editor  has 
seen  an  acute  circumscribed  swelling  which  was  not  yet  open  as  a 
fistula  and  which  was  perforated  by  an  explorer,  disclosing  a  loss 
of  alveolar  bone  and  a  small  cavity  filled  with  clear  liquid  in  the 
tissues.  The  explorer  reached  the  root  without  obstruction,  and 
no  calculus  was  present.  After  discharge  and  curettement  the 
cavities  healed.  These  two  swellings  looked  like  bKsters  or  simple 
cystic  swellings  near  the  gum  margin.  If  they  had  discharged  at 
the  gum  margin  they  might  have  produced  a  gum  pocket  simulating 
pyorrhea. 

4.  In  some  cases  of  apical  abscess  the  infection  may  travel  along 
the  pericementum  and  develop  a  secondary  abscess  at  some  point 
in  the  pericementum  (as,  for  example,  the  bifurcation),  as  a  perice- 
mental abscess.  This  form  corresponds  to  the  cases  of  Class  2,  but 
is  apt  to  be  more  acute.  It  is  also  quite  rare.  The  pulp  is,  of  course, 
dead,  at  least  partially  in  such  a  case. 


PERICEMENTAL  ABSCESS  747 

The  subject  of  pericemental  abscess  is  in  some  confusion  because 
writers  have  described  all  these  varying  phases  as  pericemental 
abscess,  which  indeed  they  are,  yet  they  require  differentiation 
into: 

1.  Cases  occurring  as  a  sequel  to  a  distinct  pyorrhea  alveolaris, 
Class  1. 

2.  Cases  associated  with  marginal  pyorrhea  cases  but  distant  to 
them,  in  all  probability  having  a  source  of  infection  in  the  pyorrhea 
pockets,  Class  2. 

3.  Cases  beginning  on  their  own  account;  the  relation  of  the  cal- 
culus if  present  as  a  cause  or  result  being  in  doubt,  Class  3  (Figs. 
658  and  659). 

4.  Cases  beginning  in  an  apical  abscess  infection,  travelling  via 
the  pericementum  to  another  portion  of  the  pericementum,  Class  4. 

Kirk's  studies  show  that  in  a  few  cases  of  pericemental  abscess 
the  pneumococcus  may  be  found  in  pure  culture.  This  suggests  a 
Class  2  case,  as  they  are  found  complicated  by  other  pyogenic  bacteria 
in  the  ordinary  pyorrheas.    A  metastatic  blood  infection  might  exist, 

Garrod  found  crystals  of  urates  in  the  serum  of  blisters  in  gouty 
patients.  In  gouty  patients  they  are  found  in  joints,  and  they  con- 
stitute the  common  tophus.  (See  p.  103.)  "Urates  of  sodium  are 
also  discharged  through  the  skin  in  gouty  abscesses,  either  in  liquid 
or  solid  form,  and  with  or  without  pus."  (Musser.)  Musser^  states 
that  a  number  of  these  abscesses  may  discharge  without  impair- 
ment of  the  general  health  or  even  with  benefit  to  the  system. 

Calculi  scraped  from  the  roots  in  pericemental  abscesses  exhibit 
in  a  varying  degree  a  response  to  the  murexid  test,  the  test  for 
urates.  (Peirce.)  The  reaction  may  be  very  faint  in  some  cases, 
being  overshadowed  by  the  calcium  phosphate  which  makes  up  the 
bulk  of  these  masses;  in  others  it  is  pronounced — i.  e.,  urates  made 
up  a  portion  of  the  deposits. 

Black^  by  test  found  urates  in  nearly  all  concretions,  salivary  and 
serumal,  about  the  teeth.  While  he  claimed  that  this  proved  that 
urates  have  no  causal  relation  to  pyorrhea,  the  findings  seem  rather 
to  point  to  frequent  presence  of  urates  in  the  salivary  and  serumal 
excretions,  which  may  really  be  a  cause  of  irritation  even  when  no 
obvious  symptoms  of  gout  are  present. 

Miller's  demonstration  of  a  calculus  upon  an  unerupted  tooth  is 
to  be  recalled.  It  seems  fairly  reasonable,  therefore,  to  suppose 
that  in  rare  cases  such  a  calculus  may  be  the  result  of  either  gout 
or  a  local  degeneration  and  act  as  an  exciting  cause.    (See  p.  312.) 

1  Medical  Diagnosis.  ^  Dental  Review,  1894. 


748 


PERICEMENTAL  ABSCESS 


Morbid  Anatomy. — Aside  from  the  state  of  the  teeth  which  show 
evidences  of  a  tendency  to  secondary  dentin  and  nodule  formation, 
it  has  been  noted  that  the  abscess  is  intrapericemental,  not  sub- 
pericemental.  Figs.  697  and  698  show  the  inflammatory  swelling  of 
the  pericementum ;  the  central  abscess  cavity,  and  the  loss  by  resorp- 
tion of  the  alveolar  process  may  easily  be  calculated.  The  original 
chronic  nature  of  the  local  irritation  in  this  case  is  evidenced  by  the 
presence  of  hypercementosis. 


Fig.  695 


Fig.  696 


A  and  C,  vital  pericementum;    B,  gouty  cal- 
culus:   D,  a  subgingival  calculus. 


A,  calculus  in  area  of  necrosis; 
B,  and  C,  vital  pericementum. 


Fig.  697 


Two  views  of  an  intrapericemental  abscess.     Pulp  vital.     (Kirk.) 


Symptoms. — These  have  been  largely  foreshadowed  in  the  dis- 
cussion of  the  pathology.  Upon  some  vital  tooth  there  appears  an 
uneasiness,  at  first  not  very  painful,  followed  later  by  an  inflamma- 


PERICEMENTAL  ABSCESS 
Fig.  698 


749 


Transverse  section  through  buccal  roots  and  pericemental  abscess  shown  in  Fig. 
G97,  showing  intrapericemental  abscess  cavity  with  fistulous  outlet  and  nearby  areas 
of  nodular  hypercementosis.     (Kirk.) 

Fig.  699 


Pericemental  abscess.     (Talbot.)     (Photograph  by  Latham.) 


750  PERICEMENTAL  ABSCESS 

tory  swelling  which  may  produce  acute  pain  and  then  discharge  a 
glairy  fluid  or  purulent  matter.  There  is  an  absence  of  the  masked 
phlegmonous  inflammatory  involvement  of  contiguous  tissues  com- 
mon in  cases  of  acute  apical  abscess.  The  flstula  may  persist  after 
the  discharge  and  the  case  may  first  be  seen  in  this  condition.  If  it 
discharges  at  the  gum  margin  it  establishes  an  ordinary  pyorrhea. 

D.  D.  Smith  calls  attention  to  the  absence  of  marked  pain  upon 
tapping  and  the  production  of  a  feeling  of  apprehension  upon  the 
part  of  the  patient  during  the  stages  preceding  the  formation  of  the 
fistula.  In  other  cases  the  shifting  of  the  tooth  from  its  position  is 
the  first  noticeable  symptom,  followed  later  by  the  pain,  and  later 
still  by  the  discovery  of  a  pocket  alongside  the  tooth. 

Diagnosis. — In  making  the  diagnosis  the  symptoms  described  are 
to  be  borne  in  mind,  but  the  disease  may  be  confounded  with  several 
diseases  having  somewhat  similar  symptoms.  An  acute  apical 
abscess  due  to  gangrenous  pulp  may  be  differentiated  by  obtaining 
evidences  of  pulp  death,  previous  root-canal  treatment,  etc.  There 
is  also  much  greater  pain  upon  percussion  than  in  pericemental 
abscess.  If  slowly  and  painlessly  formed  it  may  be  still  more  con- 
fusing, but  the  pulp  is  dead. 

Fig.  700 


A,  calculus. 

If  the  apical  abscess  be  in  the  third  stage  it  may  be  differentiated, 
if  any  doubt  exist,  by  incision  and  subsequent  exploration. 

An  acute  lateral  abscess  due  to  a  root  perforation  is  more  difficult 
of  differential  diagnosis,  but  after  incision  evidences  of  perforation 
may  be  sought  externally,  or  the  root  canal  may  be  opened.  In 
these  acute  conditions  the  a:-rays  may  render  valuable  aid.  The  pulp 
being  found  alive  by  any  reliable  test  is  evidence  that  the  case  is 
either  one  of  pericemental  abscess  or  of  acute  traumatic  perice- 
mentitis. In  a  few  cases  of  partial  gangrene  of  the  pulp  the  pulp 
may  test  as  vital,  yet  really  the  symptoms  be  due  to  apical  abscess. 


PERICEMENTAL  ABSCESS  751 

Acute  traumatic  pericementitis  usually  has  a  history  of  traumatism 
and  presents  more  pain  upon  tapping.  Any  abscess  is  usually  the 
result  of  infection  due  to  rupture  of  the  pericementum.  The  other 
forms  of  pericemental  abscess  must  be  differentiated  (see  p.  745). 

Treatment. — If  the  pericemental  abscess  discharge  by  way  of  the 
gum  margin,  infection  from  the  oral  cavity  occurs  and  the  pocket 
originally  formed  becomes  deeper.  The  case  simulates  then  a  pyor- 
rhea alveolaris  beginning  at  the  gum  margin.  The  treatment  is  then 
conducted  accordingly.  If  the  swelling  occur  upon  the  gum,  at  a 
point  more  or  less  midway  upon  the  root,  it  should  be  opened  under 
antiseptic  precautions.  An  injection  of  cocain  solution  should  be 
made,  if  necessary,  and  a  semicircular  flap  raised.  The  diseased  area 
should  be  explored  for  calculus  and,  whether  found  or  not,  the 
necrotic  tissue  should  be  curetted  away.  Next,  the  pocket  should 
be  syringed  out  with  an  antiseptic  and  filled  with  balsam  of  Peru 
or  a  clot  induced.  The  flap  is  next  laid  into  place.  The  mouth 
should  be  kept  in  an  aseptic  condition  during  the  healing  of  the 
parts.  It  is  well  to  have  the  patient  keep  the  sinus  open  with  a 
needle  to  ensure  healing  from  the  bottom  rather  than  ballooning 
by  pus,  which  may  cause  recurrences.  The  sj^stemic  considerations 
are  the  same  as  those  described  on  pp.  714  and  740. 


CHAPTER  XXVI. 
REFLEX  NEUROSES. 

Reflex  neuroses  consist  of  (1)  pain  produced  in  parts  distant 
to  the  point  at  which  irritation  is  produced,  while  pain  may  or 
may  not  be  absent  at  that  point  (sensory  reflexes),  or  (2)  they  may 
consist  of  muscular  excitation  in  parts  distant  to  the  cause  (motor 
reflexes),  or  (3)  they  may  consist  of  nutritive  disturbances  in  the 
distant  part,  probably  a  form  of  motor  reflex  in  which  the  trophic 
nerves  or  the  vasomotor  nerves  are  reflexly  irritated  so  as  to 
produce  trophic  disturbances. 

The  source  of  irritation  may  be  in  the  dentinal  fibril,  in  the  pulp, 
or  in  the  pericementum,  producing  sensory  or  motor  or  trophic 
reflexes  in  other  parts  or  the  source  of  irritation  may  be  in  some 
other  location  than  about  the  teeth  and  produce  phenomena  about 
the  face  or  teeth. 

Whether  of  dental  origin  or  not  a  sensory  reflex  is  cafled  neu- 
ralgia, though  the  cause  of  a  neuralgia  may  possibly  be  a  direct 
irritation  of  a  nerve  trunk  or  terminal. 

While  all  reflex  dental  disturbances  are,  as  a  rule,  located  in  some 
part  of  the  great  nerve  branch  supplying  the  source  of  irritation, 
the  irritation  may  be  reflected  to  distant  parts;  first,  of  the  same 
cranial  nerve,  and  secondly,  to  other  nerves.  That  is,  pain  having 
its  origin  in  one  of  the  upper  teeth  is  most  likely  to  be  referred  to 
a  point  or  points  in  the  distribution  of  the  superior  maxillary  divi- 
sion of  the  fifth  nerve.  Disturbances  in  or  about  the  lower  teeth 
are  usually  referred  to  the  distribution  of  the  inferior  maxillary 
division.  In  affections  of  either  upper  or  lower  teeth  the  pain  may 
be  referred  to  the  ophthalmic  division.  In  all  of  these  cases,  but 
most  notably  in  connection  with  disturbances  of  the  upper  teeth, 
the  usual  symptom  of  trifacial  neuralgia — tenderness  of  the  supra- 
orbital and  infra-orbital  nerves  at  their  points  of  emergence  upon 
the  face,  the  supra-orbital  and  infra-orbital  foramina — is  commonly 
present. 

Cases  are  extremely  rare  where  the  reflex  pain  is  referred  to  the 
opposite   side;    so   unusual    is    this    occurrence    that   its    mention 
warrants  suspicion  that  other  sources  of  irritation  exist  upon  the 
side  referred  to. 
( 752 ) 


REFLEX  NEURALGIA   FROM  EXPOSED  DENTIN  753 

The  extent  of  acuteness  of  reflex  pain  bears  no  direct  relation  to 
the  apparent  extent  of  the  source  of  irritation. 

As  might  be  surmised  from  the  function  of  the  dental  pulp,  painful 
reflex  dental  disorders  are  more  common  in  connection  with  diseases 
of  the  pulp  than  with  those  of  the  pericementum. 

REFLEX  NEURALGIA  FROM   EXPOSED   DENTIN. 

The  exposure  of  the  dentin  to  external  sources  of  irritation  is 
followed  by  reactions  governed,  first,  by  the  degree  of  sensitivity 
inherent  in  the  protoplasm  of  the  tissue;  and  secondly,  by  the  degree 
of  hypersensitivity  induced  in  it.  Reflex  disturbance  due  to  these 
irritations  is  more  common  in  the  class  of  persons  called  "  neuralgics," 
i.  e.,  in  those  whose  nervous  irritability  is  exalted,  a  condition  which 
may  remain  even  in  nervous  exhaustion  (see  p.  110).  Like  direct 
pulp  pains,  unless  actual  pressure  be  exerted  upon  the  affected 
tissue,  there  is  no  localized  pain.  In  the  absence  of  deliberate  irri- 
tation, the  pain  may  be  referred  to  any  portion  of  the.  peripheral 
distribution  of  the  fifth  nerve  upon  the  face,  but  if  an  acid  liquid, 
such  as  lemon  juice  or  vinegar,  or  sugars  be  taken  into  the  mouth, 
pain  is  excited,  which  is  referred  indefinitely  to  the  teeth  of  one  side, 
frequently  of  one  jaw.  Reflex  pains  due  to  this  cause  often  appear 
when  there  is  but  little  loss  of  dentin. 

When  carious  cavities  have  proceeded  to  any  depth  evidences  of 
direct  pulp  disturbance  are  obtained  through  the  increased  response 
to  thermal  changes. 

Reflex  pains  from  exposed  dentin  appear  most  commonly  in  con- 
nection with  exposures  at  the  neck  of  the  tooth  and  upon  abraded 
areas.  Obstinate  and  persistent  neuralgia,  positively  referred  to 
another  nerve  branch,  may  apparently  owe  its  origin  to  so  slight  a 
cause  as  exposure  at  the  neck  of  a  tooth  of  a  line  of  dentin  (Fig.  702). 
The  proof  of  the  connection  between  the  two  is  made  clear  by  a 
disappearance  of  the  neuralgia  after  the  exposed  dentin  has  been 
subjected  to  the  action  of  powerful  caustics  (especially  silver  nitrate), 
destroying  the  dentinal  filaments  to  some  depth.  The  connection 
between  the  two  may  be  revealed  only  by  accident;  the  contact  of 
a  toothpick,  a  dental  instrument,  or  the  finger-nail  may  induce  a 
paroxysm  of  pain.  In  one  case,  after  removal  of  calculus,  the  necks 
of  the  lower  incisors  became  a  cause  of  severe  neuralgia,  compelling 
the  use  of  silver  nitrate. 

While  in  some  cases  the  dental  origin  of  reflex  pain  may  be  made 
clear  by  the  induction  of  a  painful  response  in  the  area  of  reflection, 
by  irritating  a  tooth  pulp,  this  reaction  is  not  constant.  The  causal 
48 


Fig.  701. — Plan  of  the  fifth  cranial  nerve,  showing  the  relationships  of  the  dental 
nerves.    (After  Flowers.) 


REFLEX  NEURALGIAS  FROM  PULP  DISEASES  755 

relation  is  only  certain  when  the  cure  of  localized  dental  disease 
is  followed  by  a  disappearance  of  the  neuralgia  without  further 
treatment.      This    proof   should 
be  exacted  in  all  cases.  ^^^-  ''^^ 

The  most  common  sources  of 
neuralgic  attacks  about  the  face 
are  diseases  of  the  eyes  and  teeth. 
In  general  terms,  diseases  of  the 
eye  give  rise  to  reflex  pains  re- 
ferred to  the  distribution  of  the      „ .      r  j    .  r  xi 

Sites  of  dentin  exposure  frequently  asso- 

first  branch  of  the  fiith  nerve ;  dated  with  reflex  pains, 

diseases  of  the  teeth  usually  cause 

reflex  pains  in  either  the  superior  or  inferior  maxillary  divisions, 
according  as  the  upper  or  lower  teeth  are  affected.  In  all  painful 
affections  of  these  nerves  attention  should  at  once  be  directed  to  the 
organs  named. 

REFLEX  NEURALGIAS  FROM  PULP  DISEASES. 

The  disturbances  require  classification  according  to  the  distance 
between  their  source  and  their  manifestations. 

In  the  Fifth  Pair  of  Nerves. — Pain  referred  to  a  different  spot 
or  area  than  its  origin  is  a  characteristic  of  all  pulp  diseases.  The 
extent  of  its  reflection  depends,  first,  upon  the  patient,  as  noted  in 
connection  with  the  reflex  pains  from  exposed  dentin;  and  secondly, 
upon  the  variety  of  pulp  disease.  In  neuralgic  patients  any  variety 
of  pulp  disease  may  cause  comparatively  distant  pains.  But,  as 
Black  has  pointed  out,^  the  general  rule  is,  that  the  more  chronic  and 
profound  degenerative  diseases  of  the  pulp  are  much  more  liable  to 
give  rise  to  distant  reflex  pains  than  are  acute  pulp  diseases. 

The  pains  of  acute  hyperemia  and  of  acute  inflammation  of  the 
pulp  are  usually  referred  to  the  region  of  the  tooth  affected,  or  to  a 
corresponding  nerve  trunk.  In  conditions  of  venous  hyperemia, 
nodular  calcifications,  chronic  inflammation,  and,  later,  pulp  degen- 
erations, the  pains  may  be  of  such  character  that  their  dental  origin 
is  only  determined  after  persistent  search.  Particularly  is  this  true 
of  the  growth  of  pulp  nodules.  The  source  of  the  reflex  pains  is  all 
the  more  obscure  from  the  fact  that  in  these  chronic  degenerations 
direct  dental  symptoms  may  be  entirely  absent,  and  are  only  elicited 
upon  the  most  searching  examination  and  exhaustive  tests.  In  some 
cases  of  pulpitis  even  removal  of  the  pulp  by  cocain  has  been  fol- 

'  American  System  of  Dentistry,  vol.  i. 


756 


REFLEX  NEUROSES 


Fig.  703 


lowed  by  a  neuralgia  due  to  irritation  of  the  nerve  trunk  in  the  pulp 
stump  at  the  apex,  ^o  proved  by  cure  through  strong  sedatives 
applied  via  the  canal.  In  one  case  the  neuritis  lasted  several  days. 
There  is  no  constancy  in  the  location  of  the  pain  due  to  any  of 
these  causes;  but  tenderness  of  the  eyeball  upon  pressure;  iritis  or 
conjunctivitis;  persistent  pain  in  the  temporal  and  anterior  auricular 
regions,  particularly  in  connection  with  pulp  diseases  of  the  lower 
posterior  teeth;  in  the  ear  itself,  a  common  site  of  the  reflex  pain 
excited  by  chronic  pulp  inflammation  and  suppuration  of  that  organ ; 
behind  the  ear,  back  of  the  lower  border  of  the  mastoid  processes, 
tender  spots  may  develop;  tenderness  to  pressure  may  appear  at 
the  supra-orbital  and  infra-orbital  or  mental  foramen,  and  about  the 
chin.    In  the  same  class  of  diseases  the  pains  may  frequently  radiate 

as  far  as  the  shoulder.  Many  of  these 
cases  receive  attention  from  the  general 
practitioner,  and  the  painful  attacks  re- 
curring at  irregular  intervals  are  relieved 
by  analgesic  remedies — phenacetin,  acet- 
anilid,  exalgin,  etc. — and  no  attention 
paid  to  a  probable  dental  source  of  the 
disorder.  It  should  be  a  routine  practice 
to  examine  the  teeth  in  cases  presenting 
pains  of  the  type  and  in  the  situations 
described.  Acute  diseases  of  the  pulp, 
including  suppuration,  notably  abscess 
of  the  pulp,  usually  have  attention  di- 
rected to  the  teeth  through  pain  induced 
by  thermal  changes,  so  that  their  diag- 
nosis is  quickly  made.  Not  so,  however,  with  the  chronic  degener- 
ative changes,  except  possibly  of  pulp  nodules;  for  if  the  pulp  is  in 
the  late  stages  of  degeneration,  it  may  require  repeated  applications 
of  cold  and  heat  to  elicit  a  response  from  teeth  which  do  not  respond 
by  tenderness  upon  percussion. 

Failing  to  obtain  evidence  of  pulp  disorders,  examination  should 
be  made  for  exposed  and  hypersensitive  dentin.  Then,  examination 
of  the  pericemental  reaction  of  each  tooth  should  be  made,  and  for 
any  evidences  about  the  teeth  pointing  to  pericemental  disturbance. 
(See  later.) 

Lauder  Brunton^  records  that,  in  his  own  case,  temporal  neuralgia 
accompanied  by  tender  eyeball  was  found  due  to  exposed  dentin 
upon  the  posterior  cervical  surface  of  a  lower  third  molar  (see  Fig. 
702).    The  same  writer-  announces  that  "  so  frequently  are  headaches 


Spots   of   tenderness   in   reflex 
neuralgias  of  dental  origin. 


1  St.  Bartholomew's  Hosp.  Rep.,  voL  xix.    Reprinted  in  his  Disorders  of  Digestion. 
»  Ibid. 


REFLEX  PAINS  FROM  DISEASES  OF  THE  PERICEMENTUM     757 

dependent  upon  decayed  teeth,  that  in  all  cases  of  headache  the 
first  thing  I  do  is  to  carefully  examine  the  teeth;"  as  should  every- 
one else.  Upson  cites  by  radiograph  a  case  of  severe  headaches  of 
years  standing,  cured  by  extraction  of  an  impacted  cuspid.'  Brunton 
explains  the  painful  reaction  upon  the  accepted  hypothesis  of  the 
pathology  of  megrim,  that  it  is  due  to  spasmodic  contraction  of  the 
peripheral  end  of  an  artery,  with  dilatation  of  the  proximal  portion. 
"Irritation  in  the  tooth  is  reflected  to  the  cervical  sympathetic 
gangha  and  causes  spasmodic  contraction  of  the  arteries  through 
irregular  stimulation  of  the  vasomotor  nerves." 

An  abnormal  tooth  located  in  the  anterior  floor  of  the  nasal  cavity 
was  the  cause  of  headache  for  years,  so  proved  by  cessation  of  head- 
ache after  its  surgical  removal. 

REFLEX  PAINS  FROM  DISEASES  OF  THE  PERICEMENTUM. 

As  a  general  rule,  pericemental  pains  are  located  at  the  affected 
tooth;  but  in  some  of  the  disorders  the  teeth  may  not  be  tender  upon 
percussion,  and  yet  excite  reflex  pains  in  other  parts,  the  proof  of 
the  connection  being  determined  by  a  disappearance  of  the  pain 
upon  extraction  of  the  tooth.  The  roots  in  such  cases  usually  present 
either  an  hypertrophy  of  cementum  or  show  that  resorption  of  a 
portion^t  may  be  a  major  portion — of  the  root  has  occurred. 

In  cases  of  hypercementosis  it  is  assumed  that  the  source  of  the 
irritation  is  pressure  upon  the  nerves  of  the  pericementum  by  the 
hypertrophic  growth.  Very  widespread  disorders  may  arise  from 
this  source. 

Flagg^  records  many  varieties  of  trifacial  neuralgia;  pains  in  remote 
parts  of  the  body;  grave  functional  disorders  of  the  eye  and  ear; 
and  motor  disturbances — chorea,  epilepsy,  and  paralysis — having  a 
direct  demonstrable  connection  w^ith  hypercementosis.  Insanity  has 
also  been  produced. 

He  mentions  violent  attacks  of  trifacial  neuralgia  as  the  most 
common  reflex  disturbance  from  this  source ;  and  next,  long-continued 
pains  in  the  ear  or  eye  of  the  aftected  side.  The  existence  of  acute 
disease  of  these  organs  is  usually  diagnosticated  by  the  general 
practitioner.  He  states  that  aural  and  ocular  disturbances,  both 
functional  and  painful,  are  of  gradually  increasing  severity. 

In  examining  for  a  dental  source  of  such  pains,  exposed  dentin, 
pulp  diseases,  and  inflammatory  affections  of  the  pericementum 
should  be  first  excluded.    In  examinations  by  percussion  a  different 

1  Raper,  Items  of  Interest,  August,  1912,  p.  575. 

2  Dental  Cosmos,  1878. 


758  REFLEX  NEUROSES 

response  may  be  obtained  from  some  one  tooth  than  from  the  others. 
Hypercementosis  of  a  particular  tooth  may  be  suspected  by  finding 
the  gum  hne  shghtly  receded  and  the  tooth  attachment  unusually 
firm;  if,  in  addition,  vague,  heavy  dental  pains  have  persisted  at 
intervals  over  a  long  period,  the  diagnosis  is  probable.  It  is  only 
certain  when  tapping  upon  the  tooth  brings  on  a  paroxysm  of 
neuralgia,  and  a  skiagraph  actually  exhibits  the  hypertrophic 
growth.  The  remedy  is  extraction.  Any  root  fragment  left  unex- 
tracted  may  perpetuate  the  reflex  disorder.  The  writer  has  recently 
treated  a  case  of  neuralgia  due  to  a  lingual  root  of  a  left  upper  first 
bicuspid  which  was  retained  in  the  gum  after  extraction.  The  gum 
had  healed  perfectly  over  it.  It  was  only  discovered  by  the  use  of 
the  x-T&ys. 

Painful  affections  referred  to  the  neighboring  region  of  the  affected 
tooth,  or  diffused  through  the  distribution  of  the  corresponding 
nerve  trunk,  or  to  the  eye  or  ear,  may  accompany  the  process  of 
resorption  of  the  roots  of  permanent  teeth.  Gillman^  records  a  case 
where  facial  paralysis  disappeared  upon  extraction  of  a  tooth  which 
had  long  been  the  seat  of  disturbance  and  which,  upon  extraction, 
revealed  resorption  of  its  root.  In  these  obscure  cases  a  skiagraph, 
if  taken  at  once,  will  be  a  great  aid  in  the  exclusion  or  diagnosis  of 
pericemental  and  root  abnormalities. 

All  of  the  acute  or  chronic,  septic  or  non-septic,  inflammations  of 
the  pericementum  may  give  rise  to  reflex  pains.  The  most  common 
causes  of  the  reflex  pains  are  found  in  that  stage  of  pericemental 
irritation  which  antedates  acute  septic  apical  pericementitis.  Unless 
an  exacerbation  of  the  reflex  disorder,  or  symptoms  referable  to  that 
region,  be  induced  by  pressure  or  percussion  on  the  tooth,  a  causal 
relationship  is  only  made  out  by  either  relieving  an  existing  dental 
disorder  (for  example,  finding  and  curing  an  incipient  apical  abscess 
due  to  moist  gangrene),  an  a;-ray  skiagraph,  or  extracting  the  teeth. 

Cases  of  ovarian  and  uterine  neuralgia  and  sciatica  and  cases  of 
obstinate  pains  in  the  knee,  toes,  and  fingers  have  been  traced  to 
dental  irritation  of  some  one  of  the  varieties  named,  the  proof  of 
association  being  disappearance  of  the  pain  with  loss  of  the  tooth, 
though  this  is  now  not  always  necessary  for  a  cure. 

IMPACTED  TEETH  AS  A  CAUSE  OF  NEURALGIA. 

Neuralgia  of  varying  degrees  of  severity  is  a  common  accompani- 
ment of  impacted  teeth.  It  is  most  frequently  noted  in  connection 
with  eruption  of  the  lower  third  molars,  not  only  because  this  tooth 

^  Boston  Medical  and  Surgical  Journal,  1867. 


Phantom  odontalgia  759 

is  the  one  most  frequently  impacted,  but  because  of  the  anatomical 
relations  of  its  roots  with  the  inferior  dental  nerve. 

In  the  milder  forms  of  impaction,  those  in  which  eruption,  though 
delayed,  is  subsequently  completed,  the  pains  are  commonly  local- 
ized and  associated  with  but  occasional  attacks  of  rigidity  of  the 
masseter  muscles.  If,  however,  the  crown  present  horizontally  or 
nearly  so,  and  its  progress  is  arrested  by  impaction  against  the 
posterior  wall  of  the  lower  molar,  or  if  its  progress  be  arrested  by 
permanent  imprisonment  of  the  advancing  crown  between  the  pos- 
terior surface  of  the  second  molar  and  the  base  of  the  coronoid 
process,  not  only  may  intense  local  pains  be  induced,  but  severe 
reflex  disturbances  of  both  a  sensory  and  motor  character  may  occur. 
In  some  of  these  cases  root  formation  is  completed,  although  the 
crown  of  the  tooth  does  not  advance,  in  which  case  compression  of 
the  inferior  dental  canal  and  its  contents  may  occur  and  cause  grave 
reflex  disturbances.  The  local  irritation  about  the  root,  due  to  root 
growth,  may  excite  continued  constructive  action  by  the  peri- 
cementum, and  the  hypertrophic  growth  in  its  turn  may  be  the 
source  of  reflex  neuralgias. 

Complete  imprisonment  of  the  entire  tooth  has  been  found  to  be 
the  exciting  cause  of  facial  neuralgias,  for  the  cure  of  which  extensive 
surgical  operations  have  been  performed. 

Impacted  cuspids  and  other  teeth  may  excite  no  other  symp- 
toms than  reflex  neuralgia.  The  possible  connection  between  an 
impacted  tooth  and  neuralgia  is  made  out  after  excluding  othei- 
dental  causes,  when  it  may  be  observed  that  one  or  more  of  the 
permanent  teeth  are  absent  from  the  dental  arch,  at  dates  long  after 
their  normal  time  of  eruption. 

A  condition  equivalent  to  partial  impaction,  in  which  dental  irri- 
tation may  be  the  source  of  reflex  neuralgia,  is  seen  when  the  teeth 
are  crowded  into  arches  too  small  for  their  accommodation.  During 
the  period  of  eruption  severe  maxillary  pains  may  recur  at  intervals. 
The  diagnosis  is  by  means  of  the  .T-rays.  The  production  of  insanity 
as  a  reflex  condition  has  been  discussed  on  pp.  294  and  762. 

PHANTOM  ODONTALGIA. 

This  is  a  form  of  neuralgia  in  wdiich  symptoms  similar  to  tooth- 
ache appear  in  the  edentulous  jaws  or  in  locations  from  which  teeth 
have  been  extracted.  The  name  was  applied  by  J.  Foster  Flagg. 
It  seems  to  be  due  to  the  compression  of  nerve-endings  by  dense 
bone.  It  may,  of  course,  be  a  reflex  neurosis  from  some  other  focus 
of  pulp  or  pericemental  or  nerve  trunk  irritation. 


760  REFLEX  NEUROSES 

Any  history  obtainable  of  a  previous  local  inflammation  should 
be  obtained,  and  if  the  pain  is  localized  in  any  spot  the  bony  tissue 
may  be  broken  up  by  operation  with  a  view  to  removal  of  such  a 
cicatricial  inclusion  of  nerve  terminals.  At  least  in  troublesome 
cases  such  a  simple  operation  is  admissible.  Cryer  reports  successful 
operations  for  removal  of  "bone  whorls,"  the  cause  of  neuralgia 
(see  Fig.  704). 

Fig.  704 


The  arrow  points  to  a  dark,  three-sided  shadow — a  bone  "whorl."  The  X  on  the 
shadow  is  caused  by  a  scratch  on  the  negative.  (Radiograph  by  Pancoast.  Courtesy 
of  H.  R.  Raper.) 


PARALYSIS  OF  THE  SENSORY  TRACTS. 

The  operation  of  extraction  and  occasionally  disease  of  the  pulp 
and  pericementum  have  produced  a  temporary  paralysis  of  a  branch 


MOTOR  DISTURBANCES  FROM  DENTAL  DISEASES        761 

of  the  fifth  pair  and  loss  of  sensation  in  the  lip  or  cheek  may  result. 
So  far  as  observed  the  cases  are  of  not  more  than  a  few  months' 
duration  and  may  be  ameliorated  by  massage,  either  passive  or 
vibratory  or  by  faradization. 

MOTOR  DISTURBANCES  FROM  DENTAL  DISEASES. 

Motor  disturbances  due  to  dental  irritation  may  occur  as  recurrent 
or  persistent  contraction  or  paralysis  of  muscles,  together  with  more 
or  less  chorea;  in  rare  instances  epilepsy  and  hystero-epilepsy. 
Twitching  of  muscles  of  the  affected  side  of  the  face,  ranging  from 
slight  affection  of  the  occipitofrontalis  or  orbicularis  palpebrarum 
to  recurring  spasm  of  the  elevators  and  depressors  of  the  lower  lip, 
are  far  from  uncommon  phenomena  attendant  upon  pulp  and  peri- 
cemental diseases.  In  one  case  mentioned  by  Guilford^  a  pulp 
nodule  was  the  cause  of  tic  douloureux  (painful  muscluar  contrac- 
tions) of  two  years'  standing.  Varney  Barnes  cites  a  case  of  "  blinking 
of  the  eyes,"  caused  by  an  impacted  tooth.^  A  case  of  recurrent 
epileptic  attacks  was  proven  due  to  a  tooth  brush  bristle  forced  into 
the  gmn.^    (See  also  p.  464.) 

Contraction  of  the  masseter  muscle  is  a  common  accompaniment 
of  retarded  eruption  of  the  lower  third  molar,  which  may  be  inten- 
sified until  the  condition  is  fitly  termed  trismus,  in  some  cases  of 
partial  impaction  of  the  teeth.  Partial  trismus  has  been  found  due 
to  a  general  overcrowding  of  the  dental  arch.*  Records  of  cases  of 
torticollis,  due  to  dental  diseases,  are  also  given  by  Brubaker. 

Cases  of  facial  paralysis,  and  cases  of  paralysis  of  one  arm,  of 
paraplegia  and  hemiplegia,  and  even  of  general  paralysis,  have  been 
noted  as  disappearing  after  the  extraction  of  diseased  teeth.  It  is 
noteworthy  that  in  these  cases,  as  well  as  in  several  cases  of  tetanus 
recorded,  the  probability  of  an  infection  entered  into  the  patho- 
genesis of  the  nervous  diseases. 

Stellwagen^  records  a  case  where  symptoms  of  partial  hemiplegia 
followed  upon  the  operation  of  capping  the  pulps  of  two  molar  teeth; 
the  symptoms  disappeared  promptly  upon  extraction  of  these  teeth. 
A  case  of  facial  paralysis  followed  extraction  of  seven  roots  upon  one 
side.  It  was  successfully  treated  by  eight  applications  of  a  weak 
galvanic  current.^  Facial  paralysis  has  also  followed  the  eruption 
of  teeth,  as  of  a  second  molar.  Infantile  paralysis  has  also  been 
caused  by  dentition  (see  p.  203). 

1  Private  communication.  ^  Raper,  Items  of  Interest,  August,  1912,  p.  575. 

3  Dental  Cosmos,  1910,  p.  594. 
^  Brubaker,  American  System  of  Dentistry. 
Private  communication.  ^  Griefswald:  Cosmos,  1906,  p.  356. 


762  REFLEX  NEUROSES 

Cases  of  insanity  arising  from  dental  diseases  have  been  recorded; 
they  were  both  maniacal  and  melancholic.  In  several  of  them  a 
restoration  to  a  normal  mental  state  followed  promptly  upon  removal 
of  the  offending  teeth.  In  some  of  these  cases  a  preexisting  maxillary 
neuralgia  directed  attention  to  the  teeth  as  possible  sources  of  the 
nervous  diseases. 

Dr.  E.  Ballard  Lodge^  reports  a  case  from  the  practices  of  Drs. 
Upson  and  Stephan  in  which  a  lady  had  suffered  from  acute  melan- 
cholia and  insomnia.  A  skiagraph  revealed  an  impacted  upper 
third  molar  pressing  against  the  distal  side  of  the  second  molar. 
Extraction  effected  a  cure.  Upson^  reports  a  number  of  like  cases, 
as  well  as  some  due  to  pulp  and  pericemental  disease.  The  local 
conditions  were  painless.     (See  p.  294.) 

Cases  of  deafness  have  been  recorded  due  to  diseases  of  both  pulp 
and  pericementum,  notably  to  hypercementosis.  Deafness  which 
has  persisted  for  a  long  period  has  been  markedly  lessened  by  the 
extraction  of  teeth  the  seat  of  disease.  Cases  of  suppurative  otitis 
media  have  been  regarded  as  having  pathological  association  with 
septic  diseases  about  the  teeth,  from  the  fact  that  the  aural  trouble 
subsided  immediately  after  extraction  of  the  diseased  teeth. 

Sensory  disturbances  of  the  eye,  associated  with  dental  diseases, 
have  been  alluded  to;  in  addition  to  these,  grave  structural  and 
functional  diseases  of  the  eye,  traceable  to  dental  causes,  have  been 
recorded,  such  as  motor  and  trophic  disorders."*  Among  the  latter 
may  be  mentioned  corneal  inflammation  and  ulceration  and  phlyc- 
tenular conjunctivitis.  These  are  probably  due  in  part  to  reflex 
trophic  disturbances. 

Irregular  paralyses  of  the  third,  fourth,  and  sixth  nerves  of  the 
affected  side  have  been  noted. 

Amblyopia  and  functional  blindness  without  retinal  conditions 
to  account  for  it  have  been  found  to  arise  from  notably  advanced 
degenerative  changes  in  the  dental  pulp,  sight  returning  to  the  eye 
after  loss  of  a  diseased  tooth.  DeWitt^  records  a  most  instructive 
case  where  temporary  blindness  was  associated  with  septic  apical 
pericementitis,  disappearing  after  evacuation  of  the  abscess  and 
reappearing  when  secondary  inflammatory  action  arose  in  the  peri- 
cementum. The  ocular  affection  disappeared  permanently  and 
almost  entirely  with  the  loss  of  the  tooth.  The  history  of  this  case 
illustrates  the  important  causal  relationship  of  reflex  disturbances 

1  Dental  Summary,  1908.  2  Dental  Cosmos,  1910,  p.  526. 

'  See  Brubaker,  American  System  of  Dentistry,  vol.  iii,  for  very  full  and  detailed 
discussion  of  these  subjects. 

''  Quoted  by  Brunton,  Disorders  of  Digestion. 


DENTAL  PAIN  FROM  OTHER   THAN  DENTAL  SOURCES     763 

with  late  pulp  degenerations;  for  the  blindness  arose  two  months 
after  some  teeth  were  filled,  and  existed  for  twelve  years  before  the 
septic  apical  pericementitis  appeared. 

Trophic  Disturbances  following  Dental  Diseases. — Two  cases  of 
localized  alopecia  (loss  of  hair)  have  been  reported/  obstinate  during 
the  dental  disease  and  cured  by  the  cure  of  a  pulpitis  in  one  case 
and  extraction  of  a  root  for  suppurative  pericementitis  in  the  other. 
Such  cases  show  a  vasomotor  disturbance  in  the  distant  part. 

DENTAL  PAIN  ARISING  FROM  OTHER  THAN  DENTAL  SOURCES. 

Conditions  of  pain  the  reverse  of  those  discussed — i.  e.,  pain 
definitely  or  indefinitely  located  in  teeth  which  exliibit  no  morbid 
conditions  whatever — demand  occasional  attention  at  the  hands  of 
the  dentist. 

Chronic  malarial  poisoning,  as  stated  in  the  beginning  of  this 
chapter,  may  give  rise  to  periodical  attacks  of  maxillary  neuralgia. 
As  in  the  gouty  cases,  the  constitutional  cause  of  the  disturbance  is 
made  clear  through  the  therapeusis  most  effective,  viz.,  the  periodical 
recurrence  of  the  pain  leads  to  the  inference  of  a  malarial  origin,  and 
to  the  administration  of  quinin.  Anemia  and  other  conditions  in 
which  there  is  accumulation  of  products  of  metabolism  also  cause  it. 

Syphilitic  pains  in  the  jaws  have  a  pericemental  character,  and 
other  evidences  of  syphilis  are  present  which  point  to  a  diagnosis. 

Pains  in  or  about  the  teeth  are  occasional  accompaniments  of 
diseases  of  the  brain  or  its  vessels,  and  of  pregnancy  or  diseases  of 
the  uterus,  kidneys,  and  bladder. 

Disease  in  any  portion  of  the  fifth  cranial  nerve  may  cause  pain 
referred  to  the  teeth,  for  example,  inflammation  of  the  nerve  trunk, 
a  tumor  in  the  nerve,  or  a  tumor  pressing  upon  the  nerve  trunk, 
or  a  portion  of  fractured  bone  so  pressing,  or  a  cicatrix  contracting 
upon  a  nerve. 

Dental  pain  during  pregnancy,  without  any  direct  evidence  of 
dental  disease,  is  relatively  common. 

Disorders  of  the  lower  bowels,  causing  constipation,  may  give  rise 
to  pain  referred  to  one  or  more  teeth,  the  pain  ceasing  promptly 
upon  the  administration  of  an  active  evacuant. 

La  grippe  occasionally  produces  antral  empyema  or  neuralgia 
about  the  dental  region  as  one  of  its  sequelae. 

Pain  may  appear  in  one  or  more  teeth  either  with  or  without 
association  with  pain  about  the  maxillse  or  tenderness  at  the  foramina 

1  Moiinier:  Le  Laboratoire,  1907. 


764  REFLEX  NEUROSES 

of  emergence.  If  there  be  possible  causes  in  defective  teeth  or  teeth 
with  filHngs  in  which  pulp  irritation  is  a  possibility,  there  may  be 
difficulty  of  diagnosis.  There  may  be  a  history  of  an  attack  of 
influenza  or  even  of  coryza,  with  the  common  variety  of  which 
dental  pains  are  often  associated.  Abscess  in  the  maxillary  sinus 
or  other  sinuses  may  do  the  same. 

It  may  occur  after  la  grippe  has  seemed  to  have  disappeared.  The 
pain  is  at  first  generalized  over  the  entire  head,  but  gradually  local- 
ized in  one  or  several  upper  teeth,  more  frequently  in  the  second 
molar,  occasionally  the  bicuspids.  It  sometimes  is  so  severe  that 
the  patient  thinks  an  abscess  is  forming. 

There  is  almost  always  pain  in  the  molar  region  when  pressure  is 
made  upon  the  inner  alveolar  portion  of  the  hard  palate,  and  sensi- 
tivity of  the  external  alveolar  region. 

For  the  pseudoodontalgia  Roy  recommends  a  capsule  containing 
the  following: 

IJ — Antipyrin gr.  vij 

Quinine  hydrobromid        . gr.  iij 

Sodium  bicarbonate gr.  iij 

Sig.- — One  dose.    Increase  and  prescribe  four  times  a  day. 

Locally  he  recommends : 

I^ — Mentholis gr.  x 

Acidi  borici 5iij 

Vaselini Sj— M.  _ 

Sig. — ^A  small  portion  to  be  applied  within  the  nostrils  on  rising  and  retiring. 

Treatment  of  Facial  Neuralgia. — The  cause  should  be  sought  for, 
and,  if  possible,  removed.  If  due  to  disease  of  the  teeth,  these  should 
be  relieved;  if  due  to  eye  disease,  or  other  cause,  this  should  receive 
attention.  Should  one  not  discover  the  cause,  yet  desire  to  afford 
a  relief  pending  its  discovery,  the  accepted  remedies  antipyrin, 
acetanilid,  and  phenacetin,  combined  with  caffein  or  the  bromids, 
are  useful. 

I^ — Antipyrini  (vel  phenacetini  vel  acetanilidi)      .      .      .      .      3J 

Caffeinse  citratis gr-  x 

Potassi  bromidi 3iij — ^M. 

Ft.  in  chart  No.  x. 

Sig. — One  every  thirty  minutes  until  relieved.     (Hare.) 

If  the  patient  be  constipated,  the  bowel  should  be  freed  of  toxic 
substances  by  the  use  of  castor  oil,  repeated  as  necessary.  Castor 
oil  in  small  doses  is  antineuralgic. 

In  obstinate  neuralgia  and  other  painful  affections  with  unremov- 
able cause,  the  application  of  the  .T-rays  has  been  urged  by  Morton 
as  highly  efficacious  in  relieving  pain,  often  for  a  considerable  time. 


TREATMENT  OF  FACIAL  NEURALGIA  765 

The  blue  ray  is  also  used.  A  remedy  of  exceedingly  simple  nature 
was  introduced  by  Verge  and  Pitres  in  1902.  It  consists  of  injecting 
into  the  mucous  membrane  or  skin,  about  where  the  pain  seems  to 
originate,  1  c.c.  of  alcohol  (85  per  cent,  plus  1  per  cent,  cocain  is 
preferred  by  Lenson)  at  the  temperature  of  60°  C.  by  means  of  a 
hypodermic  syringe.    Asepsis  must  be  provided  for. 

A  slight  humming  sensation  and  swelling  of  tissue  occurs  about  the 
area  of  injection.  The  pain  disappears  for  a  long  period  after  one 
or  two  injections  a  w^eek  apart. 

Dr.  H.  I.  Patrick^  recommends  the  injection  in  trifacial  neuralgia 
not  dependent  upon  recognizable  conditions  as  preferable  in  the 
middle  aged  and  aged  to  the  Gasserian  operation,  and  sets  forth 
the  landmarks  as  well  as  the  conditions  for  the  operation. 

The  Gasserian  ganglion  has  also  been  injected  with  alcohol  with 
apparent  satisfaction,  and  is  less  serious  than  radical  operation. 

A  deep  injection  into  the  nerve  trunks  has  high  medical  indorse- 
ment. A  case  in  which  the  face  became  black  on  the  side  of  injec- 
tion was  also  followed  by  relief  and  subsidence  of  the  congestion. 
The  method  has  been  objected  to  by  some.  It  has  been  recorded 
that  myosis,  and  prickly  or  tingling  sensation  or  paralysis  of  the  part 
or  nearby  muscles  of  temporary  nature  are  by-effects.  Injection 
of  the  nerve  trunk  with  dilute  osmic  acid  has  been  practised  by 
surgeons. 

Strychnin  in  fairly  large  doses  has  been  employed  under  medical 
supervision.  When  the  cause  cannot  be  determined  the  nerve  itself 
may  be  resected.   These  are  mainly  measures  in  the  hands  of  surgeons. 

1  Journal  of  the  American  Medical  Association,  January  20,  1912. 


CHAPTER  XXVII. 

INFECTIONS  OF  AND   FROM  THE  MOUTH,  AND 
STERILIZATION. 

The  conditions  found  in  the  human  mouth,  as  pointed  out  in 
Chapter  III,  are  of  a  character  which  afford  lodgement  to,  and 
opportunities  for  multiphcation  of,  many  forms  of  bacteria,  both 
saprophytic  and  parasitic.  The  oral  conditions  are,  however,  not 
entirely  constant,  so  that  at  different  periods  they  may  favor  the 
development  of  some  special  bacterial  forms  more  than  others.  The 
nature  of  these  variations  has  not  been  made  out,  although  their 
effects  are  indubitable.  Again,  the  oral  bacterial  inhabitants  are 
not  constant  as  to  species,  for  while  there  are  many  forms  which 
appear  to  be  invariable  occupants  of  the  oral  cavity,  many  patho- 
genic forms  are  but  accidental  residents.  Becoming  resident,  they 
may  or  may  not  develop  according  as  they  find  in  the  mouth  a  suit- 
able soil.  The  nature  of  what  constitutes  a  suitable  or  unsuitable 
soil  has  not  been  determined,  although  in  some  cases  extra- oral 
culture  experiments  furnish  some  indications. 

Bacterial  growths,  as  causes  of  dental  caries  and  diseases  of  the 
pulp  and  pericementum,  have  been  discussed  in  connection  with 
those  several  diseases.  It  was  shown  that  the  pyogenic  cocci  are 
almost  constant  inhabitants  of  the  human  mouth.  There  appeared 
also  evidence  that  some  important  disorders  of  distant  parts  are 
directly  traceable  to  septic  processes  about  the  teeth,  and,  in  addition 
to  these,  suppurative  diseases  in  other  parts  become  curable  after 
removal  of  a  septic  tooth,  such  conditions  representing  infection  from 
a  local  dental  infection,  an  important  aspect  of  dental  pathology. 

Of  the  many  oral  bacterial  forms,  some  are  cultivable  and  some 
are  not;  hence  the  specific  effects  of  some  are  discovered,  others  are 
doubtful. 

With  regard  to  local  affections,  other  than  those  described  in  the 
body  of  this  book,  a  bacterial  causation  has  been  made  out  in  some, 
but  in  others  it  has  not. 

STOMATITIS. 

Definition. — By  stomatitis  is  meant  an  inflammation  of  the  mucous 
membrane  of  the  mouth.  If  secretion  is  markedly  increased  it  may 
be  termed  catarrhal  stomatitis. 

(766) 


STOMATITIS 


767 


Varieties. — It  may  be  localized,  as  in  marginal  gingivitis,  or  be 
diffuse;  and,  again,  be  accompanied  by  localized  tissue  destructions — 
ulcerations;  the  character  of  the  ulceration  differs  according  to  its 
probable  causes. 

Occurrence.^ — Most  of  these  diseases  belong  to  the  period  of  child- 
hood, although  localized  ulcerative  stomatitis  may  appear  in  the 
adult. 

Causes. — The  causes  of  stomatitis  are  so  many  and  varied  as  to 
suggest  a  classification  under  heads  according  to  assignable  causes. 
While  it  is  true  that  bacterial  infection  has  not  been  shown  to  be  a 
direct  cause  of  all  of  these  conditions,  some  degree  of  causal  relation- 
ship is  probable  in  all  of  them.  The  disease  may,  however,  be 
included  under  two  heads  according  as  they  are  or  are  not  localized, 
and  necrotic.  The  less  localized  cases  appear  as  a  diffuse  catarrhal 
affection,  affecting  wide  areas  of  the  oral  mucous  membrane;  the 
others  appear  as  spots  of  localized  tissue  destruction  attended  by 
surrounding  hyperemia. 


Catarrhal  stomatitis    { 


Local 


Symptomatic 


Simple. 

Infective 

Eruptive  fevers. 
Syphilis. 
Tuberculosis. 
Typhoid  fever. 

Drug  action 


Fermentations. 

Diphtheria. 

Gonorrhea. 


|odids. 
Mercury. 
Lead. 
Pilocarpin,  etc. 


Ulcerative  stomatitis 


Local 


Symptomatic 


Aphthae. 

Thrush. 

Noma  and  gangrenous  stomatitis. 

Herpes. 

Syphilis  (primary). 

Gonorrhea. 

Vincent's  angina. 

Stomatitis  epizootica. 

Actinomycosis. 

Lukwig's  angina. 

/  Secondary. 

\  Tertiary. 
Scurvy. 


Syphilis 


Simple  Local  Catarrhal  Stomatitis. — The  general  symptoms  of 
catarrhal  inflammation — heat  and  swelling,  with  deepened  color  of 
the  mucous  membrane,  followed  by  increased  secretion  and  exuda- 
tion— attend  several  types  of  oral  irritation,  such  as  the  irritation 
induced  by  erupting  teeth,  particularly  of  the  deciduous  teeth.  In- 
flammation of  any  degree  may  follow  the  taking  into  the  mouth 
of  caustic  chemical  substances,  such  as  caustic  alkalies,  mineral 
acids,  carbolic  acid,  etc.,  which  are  occasionally  taken  by  children. 


768  INFECTIONS  OF  AND  FROM   THE  MOUTH 

Other  irritant  drugs  and  very  hot  fluids  may  produce  similar  results. 
General  catarrhal  stomatitis  is  a  frequent  affection  of  confirmed 
smokers,  and  of  drinkers  of  distilled  liquors. 

The  cure  of  these  conditions  consists  in  the  removal  or  neutrali- 
zation of  the  cause,  and  the  use  of  local  sedatives  and  antiseptics  to 
allay  irritation  and  prevent  infection.  The  most  effective  method 
of  treating  the  inflammatory  condition  is  by  antiseptic  sprays,  such 
as  diluted  Dobell's  solution,  followed  by  sprays  of  strong  solutions 
of  potassium  chlorate.  If  much  pain  exist,  phenol-sodique  is  an 
admirable  sedative  antiseptic,  used  in  10  to  20  per  cent,  solution,  as 
a  spray. 

Infective  Local  Catarrhal  Stomatitis. — This  in  some  degree  is  a 
common,  perhaps  the  necessary,  antecedent  condition  to  many  of 
the  ulcerative  forms  of  stomatitis.  It  is  probable  that  many  of  the 
cases  of  stomatitis  found  in  infants,  children,  and  adults  are  due  to 
unusual  fermentations  occurring  in  the  mouth.  Children  whose 
nursing  bottles  are  not  kept  clean;  those  who  at  a  later  age  suffer 
from  neglect  of  the  teeth  and  from  the  effects  of  improper  food: 
adults  in  whose  mouths  dental  disease  is  widespread,  and  whose 
oral  hygiene  is  very  faulty;  all  exhibit  abnormal  conditions  of  the 
oral  mucous  membrane — more  or  less  swelling,  softness,  and  deepened 
color  of  the  mucous  membrane,  a  coated  tongue,  and  offensive 
breath,  with  an  increase  of  oral  secretions. 

The  complexus  of  oral  symptoms  is  commonly,  and  also  by  the 
general  practitioner,  regarded  as  symptomatic  of  gastric,  intestinal, 
and  hepatic  disorders,  as  doubtless  it  is,  but  the  causal  relation- 
ship is  in  many  cases  probably  the  reverse  of  that  implied  in  such 
opinions,  for  it  is  probable  that  the  disturbances  of  digestion  are 
fermentative  in  character,  and  the  organisms  causing  them  find  their 
way  to  the  stomach  from  the  mouth,  which  was  first  affected.  The 
treatment  of  this  condition  consists  in  the  correction  of  its  causes, 
their  non-repetition,  and  the  continued  use  of  oral  antiseptics. 

Symptomatic  Catarrhal  Stomatitis. — Stomatitis  in  its  catarrhal 
form  usually  accompanies  the  early  and  later  stages  of  the  eruptive 
fevers,  scarlet  fever,  smallpox,  etc.  In  scarlet  fever,  smallpox,  and 
measles  evidences  of  direct  infection  of  the  mouth  exist  and  the  in- 
flammatory reaction  is  pronounced. 

Catarrhal  stomatitis  is  one  of  the  manifestations  of  secondary 
and  tertiary  syphilis,  antedating  the  appearance  of  tissue  necrosis 
(ulcerations). 

More  or  less  catarrhal  stomatitis,  confined,  it  may  be,  to  the 
mucous  membrane  of  the  gums,  is  common  in  the  mouths  of  phthi- 
sical patients;     tubercular  ulcers  may  arise  or  threaten.     In  some 


STOMATITIS  769 

cases  the  palate  has  been  perforated.  Curtis  states  that  these  are 
usually  fatal. 

The  stomatitis  of  typhoid  fever  may  be  regarded  as  an  almost 
essential  feature  of  the  disease. 

The  eflPects  of  drug  elimination  by  the  oral  tissues  have  been 
already  discussed  (see  p.  648  and  773). 

Mercurials  in  excess  produce  gingivitis  with  puffy  gums  which 
bleed  readily;  there  is  coated  tongue,  fetid  breath  in  marked  cases, 
swollen  tongue  and  cheeks,  and  exfoliation  of  the  teeth.  The  history 
of  administration  of  mercurials,  and,  possibly,  of  syphilis,  as  a  reason 
for  it  affords  a  diagnosis.  The  mercury  should  be  stopped;  atropin 
sulphate,  5  minims  of  a  1-grain  to  1-ounce  solution  in  water,  admin- 
istered as  an  antisialagogue  every  four  to  six  hours;  a  5  per  cent, 
potassimn  chlorate  solution  in  hydrogen  dioxid  makes  a  useful 
mouth  wash  for  reducing  the  local  inflammation. 

Ulcerative  Stomatitis. — In  all  probability  these  ulcerations  are 
always  infective.  Like  catarrhal  stomatitis  the  ulcerative  disease  may 
have  only  a  local  significance  or  be  indicative  of  some  general  disease. 

Ulcerative  Stomatitis  of  Local  Significance. — The  more  usual  or 
infantile  forms  of  these  disorders  are  a  sequel  of  catarrhal  stomatitis, 
at  least  of  an  acquired  debility  of  the  oral  tissues,  and  their  primary 
cause  is,  therefore,  the  cause  producing  a  condition  of  mucous  mem- 
brane which  permits  the  growth  of  infective  organisms.  One  of  these 
diseases,  thrush,  has  already  been  described.  The  others,  aphthae, 
herpes  labialis,  and  noma,  are  all  probably  due  to  the  action  of 
organisms. 

Aphthae. — This  affection  is  common  in  its  isolated  form,  as  the 
canker  sore.  In  the  catarrhal  stomatitis  of  children,  during  or  after 
dentition,  multiple  sores  frequently  make  their  appearance.  The 
condition  can  best  be  studied  when  it  appears  as  an  isolated  sore  in 
the  mouth  of  the  adult.  The  most  common  situation  of  the  sore  is 
at  the  junction  of  two  mucous  surfaces,  such  as  that  of  the  gum  with 
the  lip  or  cheek,  or  that  of  the  floor  of  the  mouth  with  the  gmn  or 
tongue.  Redness  diffused  over  a  limited  area,  followed  by  a  nodular 
hardening,  occurs,  during  which  local  pain  is  annoying;  the  centre 
of  the  hardened  area  breaks,  the  epithelium  disappearing,  forming  a 
raw  surface,  which  quickly  acquires  a  rough,  yellowish  white  coating 
which  is  easily  removable.    The  sores  are  very  painful. 

The  mouth  is  usually  otherwise  healthy,  and  there  is  an  absence 
of  associated  throat  and  skin  affections. 

The  notable  fungus  of  the  blastomycetes  is  the  saccharomyces 
albicans;  this  organism,  when  classified  by  mycologists  as  a  thread 
fungus,  was  known  as  the  oidium  albicans  (Fig.  705).  The  gro\\i:h 
49 


770 


INFECTIONS  OF  AND  FROM   THE  MOUTH 


of  this  organism  illustrates  forcibly  the  influence  of  soil  on  the 
growth  of  fungi.  It  does  not  occur  in  the  mouths  of  healthy,  well- 
nourished,  and  clean  children  with  good  surroundings.  It  is  a  disease 
of  childhood,  particularly  of  nurslings,  and  its  occurrence  is  almost 
always  confined  to  bottle-fed  babies  whose  feeding  bottles  are  kept 
in  an  unclean  condition.  Debility  of  the  oral  tissues  is  established 
in  consequence  of  the  fermentations  arising  from  the  source  just 
named,  furnishing  a  favorable  condition  for  the  development  of  the 
saccharomyces  (oidium)  albicans.  The  condition  produced  is  known 
as  thrush.  The  infection  may  be  carried  from  one  child  to  another, 
and  if  the  fungus  be  brought  in  contact  with  an  abraded  mucous 
surface  of  an  adult  it  may  develop. 

The  fungus  burrows  between  the  epithelial  cells  of  the  mucous 
membrane  (Fig.  706),  not  beyond  it.  It  first  appears  in  small  spots 
which  coalesce,  until  large  patches  of  a  membranous-like  growth 


Fig.  705 


Fig.  706 


Saccharomyces  albicans,  thrush  fungus. 
(Miller.) 

cover  extensive  surfaces,  spreading 
by  continuity  to  all  of  the  mucous 
surfaces  associated  with  the  mouth. 

As  bud  fungi  flourish  only  in 
media  of  acid  reaction,  the  use  of 
alkaline  washes  is  indicated  in 
the  treatment  of  this  condition. 
Wiping  the  patches  with  dilute 
phenol-sodique  is  efficacious.  Small 
spots  may  be  cauterized  with  silver 
nitrate  or  trichloracetic  acid. 

Hydrogen  dioxid  or  25  per  cent, 
iodin  in  glycerin  are  also  useful. 

This  condition  follows  so  constantly  upon  the  taking  of  very 
indigestible  food,  such  as  lobster,  Welsh  rarebit,  etc.,  that  acute 
indigestion  must  be  regarded  as  having  some  causal  relationship 


Pavement  epithelium  covered  with 
spores  of  the  oidium  albicans.  (Ch. 
Robin.) 


STOMATITIS  771 

w  ith  it.  It  is  also  of  frequent  occurrence  in  the  mouths  of  dyspeptics; 
that  form  of  gastric  disturbance  attended  with  a  deficiency  of  hydro- 
chloric acid  in  the  gastric  juice  appears  to  have  a  constant  association 
with  it,  though  it  is  probably  caused  by  the  oidium  albicans. 

The  appearance  of  ulcerative  stomatitis  in  children,  together  with 
its  treatment,  was  discussed  in  the  chapter  on  Dentition. 

The  general  treatment  of  these  ulcerations  appearing  in  the  mouths 
of  children  is  the  administration  of  a  laxative,  and  the  subsequent 
administration  of  listerine,  gtt.  x,  every  two  hours.  Locally  the 
mucous  membrane  is  to  be  sprayed  with  hydrogen  dioxid,  followed 
by  sprays  of  strong  solutions  of  potassium  chlorate. 

Localized  aphthous  patches  in  the  adult  are  promptly  relieved  by 
the  administration  of  calomel,  gr.  ij,  at  night,  followed  in  the  morning 
by  a  mild  saline.  The  local  sore  is  dried  and  touched  with  pure 
carbolic  acid.  The  administration  of  alkalies  before  meals,  and 
hydrochloric  acid  after  meals,  usually  remedies  the  gastric  condition, 
unless  it  be  of  long  standing.  A  variety  of  aphthous  sore  is  called, 
from  the  anatomical  situation  of  the  ulcers,  follicular  stomatitis. 
Irritation  and  swelling  of  the  mucous  follicles  in  the  palatal, 
buccal,  and  labial  mucous  membrane  are  accompanied  by  more  or 
less  localized  inflammation;  the  follicles  become  ulcerous,  the  small 
ulcers  having  a  uniform  size.  This  condition  quickly  disappears 
under  the  treatment  advised  for  ulcerative  stomatitis.  An  indica- 
tion of  the  bacterial  origin  of  all  of  these  disturbances  is  seen  in 
the  efficacy  of  antiseptics  used  in  their  treatment. 

Rubber  Sore  Mouth. — A  form  of  stomatitis  is  due  to  artificial 
dentures  resting  upon  the  mucous  membrane,  and  either  by  pressure 
or  light  friction,  or  possibly  by  preventing  radiation  of  heat,  they 
cause  desquamation  of  the  epithelium.  The  part  beneath  the  plate 
assumes  a  more  or  less  reddened  or  ulcerated  appearance.  Vulcanite 
plates  that  are  not  smooth  upon  their  surfaces  of  adaptation  may 
produce  this  physical  irritation,  but  oftentimes  such  surfaces  may 
covered  with  infective  mucous  plaques,  so  that  this  may  in  some 
cases  be  an  added  cause. 

Eilestein  has  shown  that  the  use  of  vermillion  colored  vulcanite 
causes  minute  pores  to  appear  in  the  vulcanite  which  harbors  bacteria 
which  may  induce  inflammation  of  the  oral  epitheliiun.^  The  use  of 
carmine-colored  vulcanite  is  suggested. 

Treatment. — The  treatment  consists  of  rest  and  healing  mouth 
washes.    Antiseptics  are  usually  included.     (See  Gingivitis.) 

Stomatitis  Aphthosa  Epizootica.^ — This  is  the  oral  expression 
of  foot-and-mouth  disease  occurring  in  cattle  and  rarely  fatal,  and 

1  L'Odontologie.    See  Dental  Cosmos,  February,  1911,  p.  248. 

2  Lartschneider:    Dental  Cosmos,  1908,  p.  880. 


772  INFECTIONS  OF  AND  FROM  THE  MOUTH 

usually  lasting  about  eight  weeks.  The  germ  is  not  fully  determined 
as  yet. 

Equinia  (Glanders) . — An  infectious  disease  of  cattle  which  may  be 
transferred  to  man,  producing  a  purulent  discharge  from  eyes,  nose, 
and  mouth. 

Diagnosis. — The  diagnosis  rests  upon  the  presence  of  the  disease  in 
nearby  cattle  and  the  prodromata  and  later  presence  of  fever,  pustules 
on  the  mucous  membranes  of  the  lips,  tongue,  and  sometimes  on 
the  hard  palate  and  throat,  occasionally  between  fingers,  around 
nails,  or  on  nipples.  These  later  burst,  leaving  ulcers  with  a  grayish- 
yellow  coating.  The  pustules  dry  up  without  scars  in  the  second  week. 

Treatment. — The  treatment  rests  upon  antisepsis  in  so  far  as  the 
local  manifestations  are  concerned. 

Diphtheria. — While  the  point  of  first  attack  of  the  diphtheria 
bacillus  is  most  marked  about  the  soft  palate  and  tonsils,  the  false 
membrane  forming  there  and  spreading  to  the  pharynx,  more  or  less 
general  inflammation  of  the  oral  mucous  membrane  also  occurs. 

NOMA,  CANCRUM  ORIS,  GANGRENE  OF  THE  MOUTH. 

In  ill-fed,  ill-nourished,  and  ill-kept  cachectic  children,  the  debili- 
tation of  the  oral  tissues  may  exceed  the  grades  given,  and  a  disease, 
probably  bacterial  in  origin,  may  arise  which  leads  to  widespread 
necrosis  of  the  cheeks  and  maxillae.  The  condition  is  called  gangrene 
of  the  mouth,  noma,  or  cancrum  oris ;  the  latter  term  has  been  applied 
to  the  less  severe  varieties. 

This  disease  may  make  its  appearance  as  an  ulcer  at  the  junction 
of  cheek  and  gum;  in  other  cases  a  severe  stomatitis  arises  without 
a  primary  ulcer.  A  greater  or  less  extent  of  the  cheek  acquires  a 
board-like  hardness,  becoming  livid;  the  overlying  mucous  mem- 
brane breaks,  exhibiting  a  large  slough.  The  necrosis  extends  toward 
cheek  and  jaw,  destroying  further  tissue.  The  sloughs  undergo 
putrefactive  decomposition,  emitting  a  stench.  The  destruction  of 
tissue  may  be  arrested,  or  may  proceed,  destroying  in  a  few  days 
the  entire  cheek  and  bony  tissues.  In  the  more  severe  cases  the 
disease  is  almost  invariably  fatal,  because  the  extent  of  the  tissue 
destruction  bears  a  constant  relation  to  the  underlying  debility  of 
the  patient.  It  will  be  seen  that  the  disease  resembles  malignant 
pustule  or  carbuncle  in  several  of  its  features. 

Schimmelbusch^  found  a  bacillus  (pure  culture)  upon  the  borders 
of  the  necrosis  which  may  prove  pathogenic  of  noma. 

'  Miller:  Dental  Cosmos,  September,  1891. 


NOMA,   CANCRUM  ORIS,   GANGRENE  OF  THE  MOUTH     773 

Hillesen  obtained  a  diplococcus  which  developed  in  pure  culture" 
produced  noma  in  an  animal  into  which  it  was  injected,  and  from 
the  lesion  a  pure  culture  of  it  was  obtained  which  in  like  manner  was 
put  through  four  animals.^ 

These  cases  are  purely  medical ;  so  that  their  full  discussion  is  not 
warranted  in  these  pages.  The  principle  of  treatment  is  to  improve 
the  general  condition  of  the  child,  destroy  the  probable  infection 
in  the  borders  of  the  still  vital  tissue  by  cauterization,  and  promote 
sloughing  of  the  necrosed  tissue  by  the  use  of  antiseptic  applications. 

Fig.  707 


Noma.     (J.  Lewis  Smith.) 


Dr.  L.  Fisher  (New  York)  reported  a  case  upon  the  inside  of  the 
cheek,  cured  by  applications  of  ichthyol  in  lanolin  four  times  a  day 
over  the  entire  area.^ 

The  Eruptive  Fevers  .^ — Hyde  and  Montgomery  describe  the  fol- 
lowing oral  symptoms  associated  with  various  diseases  having 
eruptive  dermatitis  as  phenomena: 

Scarlatina. — The  mucous  surfaces  of  the  mouth  and  fauces  are 
engorged  tumid,  reddened,  and  often  covered  with  deep  reddened 
puncta.  The  tongue  is  coated  with  a  white  fur  over  the  filiform 
papillae.  This  is  first  partly  lost,  giving  red  puncta  and  a  white 
background;  when  totally  lost  it  gives  "strawberry  tongue." 


1  Dental  Cosmos,  1908,  p.  180. 


2  Ibid.,  1902. 


774  INFECTIONS  OF  AND  FROM  THE  MOUTH 

Variola.— The  papules  may  appear  over  the  entire  ahmentary 
canal.  In  the  mouth  they  lose  their  epithelium,  through  heat, 
moisture,  and  friction.  Reddened  excoriated  surfaces  appear,  over 
which  the  epidermis  is  reformed.     Gangrenous  complications  are  rare. 

Hemorrhagic  Variola  (Effusions  of  Blood  into  Mucous  Surfaces). — 
The  mucocutaneous  orifices  are  crust-covered  and  exude  an  extreme 
fetor.     Blood  may  escape  from  the  mouth. 

Varicella. — The  macular  lesions  may  extend  to  the  surfaces  of  the 
eyes,  mouth,  etc. 

Rubeola. — Even  three  days  before  skin  eruptions.  "Koplik's  spots," 
bluish  white  or  bright  red  with  central  bluish-white  punctum  on 
mucous  membrane.  In  period  of  affloresence  a  catarrhal  or  eruptive 
inflammation. 

Syphilis. — Secondary  eruptions,  later  forming  mucous  patches; 
characteristic  crusts  about  nose  and  mouth. 

Urticaria. — The  eruption  in  well-marked  cases  may  include  the 
mucous  membranes. 

Angioneurotic  Edema. — The  rosy  red  to  livid  edematous  plaques 
may  appear  upon  the  lips  and  pharynx,  producing  at  times  dyspnoea. 

Erythema  Scarlatiniforme. — The  mucous  membranes  in  mouth 
and  fauces  may  be  reddened  or  be  denuded  of  epithelium,  but  the 
characteristic  "  strawberry  tongue"  of  scarlatina  is  wanting. 

Erythema  Iris. — The  papules  may  coalesce  and  be  filled  with 
blood  or  hematuria  may  result  with  severe  involvement  of  mucous 
membranes  of  lips  and  mouth,  ulceration  rapidly  ensuing. 

Erythema  Multiforme. — Like  the  iris  variety  the  macules  may  appear 
in  the  mouth. 

Dermatitis  Herpetiformis. — When  afl^ected,  mucous  membrane  of 
mouth  sodden,  macerated,  pustules;  and  bullae  form  and  rupture, 
leaving  raw  erosions  or  sloughing  patches  of  mucous  membrane; 
extremely  foul  odor. 

Herpes  Simplex. — Herpes  Zoster. — See  this  chapter. 

Erysipelas. — May  extend  to  mouth,  causing  a  dry,  tumid,  glazed 
appearance. 

Rhinoscleroma. — A  rare  disease;  usually  begins  in  nose;  may  extend 
to  mouth,  with  ulcerative  destruction,  causing  exfoliation  of  the  teeth. 

Pemphigus  Foliaceus. — The  mucous  membrane  of  the  mouth  and 
throat  may  be  denuded. 

Pemphigus  Vegetans. — White  patches  followed  by  excoriation  with 
foul  odor  may  occur. 

Drugs  Producing  Stomatitis. — Many  drugs  taken  internally  may 
produce  dermatitis  or  stomatitis  as  a  temporary  effiorescence,  while 
with  some,  as  mercury,  the  impression  is  more  profound  (see  p.  648) ; 


SYPHILITIC  AFFECTIONS  OF  THE  MOUTH  lib 

with  others  it  is  simply  expression  of  idiosyncrasy,  with  which  the 
oral  tissues  may  or  many  not  take  part. 

lodin  or  bromin  or  their  compounds;  antipyrin  and  others  of  its 
class;  arsenic,  belladonna,  aconite,  carbolic,  nitric,  tannic,  boric,  and 
benzoic  acids;  sodium  benzoate  and  sodium  borate. 

Chloral,  digitalis,  mercury,  opium  and  its  alkaloids,  phosphorus, 
podophyllum,  potassium  chlorate,  castor  oil,  cinchona  and  its  alkaloid, 
quinine,  salicylic  acid  and  salicylates,  strychnine,  tar,  turpentine,  and 
others  of  less  interest  are  mentioned.  Silver  nitrate  rhay  produce 
argyria  of  the  skin  and  mucous  membranes.  As  instanced  by  argyria, 
the  drug  finds  its  way  to  the  superficial  tissue  in  which  it  may 
produce  irritation. 

SYPHILITIC  AFFECTIONS  OF  THE  MOUTH. 

The  recognition  of  syphilitic  lesions  about  the  mouth  is  of  vital 
importance  to  the  dental  operator,  first,  because  by  the  recognition 
he  may  take  steps  to  prevent  the  carriage  of  infection  to  innocent 
patients;  and  secondly,  that  he  may  avoid  inoculation  of  himself 
by  the  poison. 

In  the  minds  of  many,  syphilis  is  associated  with  the  lower  class  of 
persons,  who  are  confirmed  debauches.  While  it  is  undoubtedly  true 
that  its  prevalence  is  most  marked  in  this  class  of  persons,  it  appears, 
with  horrible  frequence,  in  persons  who  would  be  little  suspected 
of  having  such  infection.  The  operator  is  to  be  guided  in  his  opinions 
and  precautions  in  this  matter,  not  by  the  social  status  of  the  patient, 
but  by  the  nature  of  the  morbid  conditions  existing. 

The  cause  of  syphilis  is  the  traponema  pallidum  discovered  by 
Schaudin  and  Hoffman,  and  present  in  its  lesions,  transmitted  from 
one  person  to  another  directly  or  through  the  medium  of  an  inani- 
mate object  which  has  been  infected. 

The  diagnosis  may  be  made  by  microscopic  examination.  The 
sore  is  washed  and  the  serum  later  exuded  used  to  make  a  smear  on 
a  glass  slide.  Stein  states  that  the  edge  of  the  sore  should  be  scraped 
with  a  sharp  instrument  after  washing,  and  the  serum  collected 
from  that  source,  otherwise  the  treponema  may  not  be  obtained.^ 
This  is  first  dried  in  the  air,  then  stained  with  Hastings'  stain.  After 
a  minute  distilled  water  is  added  until  a  metallic  film  is  formed. 
After  five  minutes  more  they  are  washed  in  running  water  and 
dried.  The  treponema  pallidum  stains  a  faint  blue.^  They  may 
also  be  seen  living  by  aid  of  the  "dark-field  illuminator." 

1  Dental  Cosmos,  July,  1913,  p.  744. 

2  McKee:    Dental  Cosmos,  1909,  p.  1437. 


776  INFECTIONS  OF  AND  FROM   THE  MOUTH 

Syphilis  is  usually  divided  into  three  stages,  primary,  secondary, 
and  tertiary;  to  these  may  be  added  a  fourth  stage,  viz.,  in  patients 
who  have  been  discharged  as  cured  mild  manifestations  of  disorders, 
particularly  of  the  skin  and  mucous  membranes,  make  their  appear- 
ance from  time  to  time,  and  disappear  promptly  upon  the  adminis- 
tration of  iodids.  The  semen  of  syphilitics  in  the  secondary  period 
is  infectious  to  apes. 

The  first  stage  of  syphilis — primary  syphilis — consists  in  the  for- 
mation of  the  primary  sore  or  chancre,  and  the  involvement  of  the 
nearest  lymphatic  glands.  Secondary  syphilis  is  attended  by  fever, 
eruptive  inflammations  of  the  skin,  inflammation  and  superficial 
ulceration  of  mucous  structures.  In  tertiary  syphilis  destructive 
inflammation  of  the  skin,  mucous  membranes,  and  connective  tissue 
occurs,  together  with  the  formation  of  speciflc  tumors — gummata. 

Some  difi^erences  of  opinion  exist  among  syphilographers  as  to  the 
relative  infective  power  of  the  secretions  from  the  several  lesions 
of  syphilis.  All  are  agreed,  however,  that  the  secretions  from  the 
secondary  lesions  observed  in  and  about  the  mouth  are  highly 
infective.  It  is  the  part  of  prudence  to  regard  all  syphilitic  lesions 
as  infective.  All  these  stages  of  syphilis  may  be  seen  in  the  human 
mouth.  It  is  to  be  remembered  that  if  the  mucous  membrane  of 
the  mouth  be  infected  from  a  mucous  patch  (a  secondary  lesion), 
the  acquired  disease  will  appear,  not  as  a  mucous  patch,  but  as  a 
chancre.  It  is  from  mucous  patches  that  infection  is  most  to  be 
feared. 

Primary  Syphilis  of  the  Mouth. — Causes. — The  primary  lesion  of 
syphilis,  chancre,  when  found  in  the  mouth  is  a  consequence  of  direct 
infection  from  a  syphilitic.  The  infection  occurs  from  contact 
of  the  mucous  surface  of  the  mouth  with  a  syphilitic  lesion  upon 
another  person.  It  has  been  transmitted  by  kissing,  even  with 
an  innocent  person  as  the  intemediary;  it  may  occur  from  using 
a  glass  or  cup  previously  used  by  a  syphilitic,  by  smoking  cigars  or 
cigarettes  which  have  been  made  by  syphilitic  cigarmakers,  who 
have  applied  the  tongue  to  the  tobacco  in  attaching  the  wrapper. 
Dental  instruments  may  be  the  carriers.  Any  of  the  articles  named, 
or  the  contact  of  any  article  which  has  been  in  contact  with  a 
syphilitic  lesion,  if  brought  in  contact  with  an  abraded  mucous  sur- 
face, may  cause  infection.^ 

The  infection  may  be  transferred  from  patient  to  operator  if  the 
fingers  have  any  abraded  surface,  or  if  the  surface  is  broken  acci- 

'  Metchnikoff  and  Roux  found  that  an  ointment  composed  of  10  parts  calomel 
and  20  parts  lanolin,  applied  by  inunction  to  an  intentionally  infected  part,  prevented 
the  appearance  of  syphilitic  infection  if  used  within  one  hour  after  inoculation.  Mer- 
curic chlorid  was  of  no  avail.     Dental  Cosmos,  1907,  p.  1007. 


SYPHILITIC  AFFECTIONS  OF  THE  MOUTH  111 

dentally  by  an  instrument.  Dentists  have  been  inoculated  upon  the 
hand.  During  and  since  the  time  of  Hunter  the  use  of  teeth  from 
syphilitic  patients  in  plantation  operations  has  been  a  clearly 
recognized  medium  of  communication.  About  32  per  cent,  of  all 
primary  chancres  appear  within  the  dental  field  either  upon  the 
lips  or  within  the  mouth. 

Appearance  and  Diagnosis. — "The  primary  lesion  of  syphilis 
never  makes  its  appearance  before  ten  days  after  infection;  the 
maximum  period  is  about  ninety  days;  the  average  is  twenty-one 
days."i 

It  usually  appears  as  a  single,  elevated,  hard  papule.  In  cases  of 
dental  infection,  most  frequently  about  the  lips,  the  papule  loses  its 
epithelial  coating  after  some  days.  The  induration  surrounding  the 
papular  mass  increases  until  the  papule,  which  is  now  raw  and  in  a 
process  of  ulceration,  appears  surrounded  by  a  ring  of  cartilaginous 
hardness.  This  induration  is  the  one  distinguishing  feature  of  the 
chancre,  which  is  not  painful.  In  about  a  week  after  the  appearance 
of  the  primary  sore,  swelling  of  the  submaxillary  lymphatic  glands  is 
observed.  In  case  the  chancre  appears  upon  the  tongue,  the  sub- 
hyoid lymphatic  glands  are  swollen. ^  Unless  pyogenic  infection  has 
occurred,  the  lymphatic  involvement  is  not  inflammatory,  there 
being  no  pain  present.  In  from  three  to  four  weeks  the  sore  disap- 
pears, leaving  no  signs  of  its  site  in  some  cases;  in  others,  some 
induration  may  persist. 

The  diagnosis  of  this  condition  is  the  important  consideration,  so 
far  as  the  dental  practitioner  is  concerned,  its  treatment  being  the 
province  of  the  medical  practitioner. 

The  elevation  of  the  sore,  its  induration,  and,  if  obtainable,  the 
time  of  inoculation,  are  diagnostic  data.  The  sore  is  single,  as  a 
rule,  and  there  is  hard,  nodular  painless  swelling  of  the  neighboring 
lymphatics.  A  single  ulcer  of  ulcerative  stomatitis  may  in  some 
degree  simulate  the  appearance  of  a  very  small  chancre.  It  may 
exhibit  slight  induration,  but  its  irregular  form,  situation,  painful- 
ness,  and  the  usual  absence  of  lymphatic  involvement,  together 
with  its  prompt  disappearance  after  sterilizing  the  mouth  and  cauter- 
izing the  ulcer,  will  differentiate  the  two  sores.  If  the  chancre  be 
upon  the  tip  or  sides  of  the  tongue,  where  it  is  subjected  to  irrita- 
tion, it  may  become  very  large  and  bear  a  close  resemblance  to 
epithelioma  of  that  organ.  In  epithelioma  there  are  apt  to  be  pains 
of  a  lancinating  character,  the  induration  follows  ulceration,  and 
the  ulcer  has  hard  edges  and  often  a  warty-like  growth. 

1  Gross:    System  of  Surgery.  ^  Park:    Surgery 


778  INFECTIONS  OF  AND  FROM  THE  MOUTH 

It  is  a  wise  precaution  to  view  all  sores  about  the  mouth  as  possibly 
infectious.  All  errors  of  diagnosis  in  this  direction  will  be  more  than 
compensated  for  by  the  assurance  of  non-transference  of  infection. 

Secondary  Syphilis  of  the  Mouth. — The  secondary  manifestations 
of  syphilis  may  be  observed  in  and  about  the  mouth,  no  matter  what 
the  location  of  the  primary  lesion  may  have  been ;  they  are  the  result 
of  a  general,  not  a  local,  infection.     A  skin  eruption  appears  also. 

Fig.  708 


Chancre  of  the  h'p. 

Secondary  infections  of  the  mucous  tissues  appear  in  from  four 
to  twelve  weeks  after  the  appearance  of  the  primary  lesion.  Sore 
throat,  due  to  inflammation  of  the  mucous  membrane  of  the  pharynx 
and  parts  about,  is  almost  constant;  together  with  syphilitic  hoarse- 
ness, due  to  the  extension  of  the  affection  to  the  mucous  membrane 
of  the  larynx. 

The  appearance  of  copper-colored  areas  upon  some  portion  of  the 
mucous  membrane,  on  the  tonsil,  pharynx,  soft  palate,  lips,  or  bucco- 
labial  surface,  precedes  the  loss  of  epithelium  over  these  surfaces, 
which  soon  occurs,  forming  the  most  virulently  contagious  lesion 
of  syphilis,  the  mucous  patch.  The  patches  become  covered  with 
a  grayish-white,  opalescent,  pasty  covering,  resembling  the  ulcera- 
tions of  non-specific  stomatitis.  So  close  is  the  resemblance  that  a 
differentiation  can  only  be  made  at  times  by  additional  evidences  of 
secondary  syphilis.  Single  patches  may  coalesce,  forming  large, 
irregular  areas  covered  by  a  grayish-white  pellicle.  These  patches 
are  rarely  painful.  Ulcerations  having  ragged,  irregular  outlines 
may  appear  at  the  sites  of  the  original  patches  or  in  other  situations, 
and  exhibit  a  tendency  to  spread.  In  healed  cases  the  cicatrices 
present  a  whitish  pellicle  and  contracted  scar,  indicative  of  old 
healed  ulcers.    In  the  skin  little  pits  and  linear  scars  are  symptomatic. 

The  diagnosis  of  the  condition  is  determined  by  the  history  and 


SYPHILITIC  AFFECTIONS  OF  THE  MOUTH  779 

by  a  discovery  of  other  lesions  of  secondary  syphilis,  iritis,  head- 
ache, neuralgia,  paralysis  of  muscles  of  eye  and  face,  chorea,  brittle, 
cracking  nails  are  often  early  symptoms  ;i  also  the  lymphatic  glands 
will  be  involved;  skin  eruptions,  falling  out  of  the  hair  (alopecia), 
and  the  areas  of  copper-colored  eruption  upon  the  mucous  mem- 
brane of  the  pharynx  and  soft  palate. 

Hugenschmidt^  has  observed  among  syphilitics,  who  presented  no 
local  lesions,  the  frequent  nocturnal  occurrence  of  indefinitely  located 
dental  pains,  spreading  to  the  palatal  region.  In  case  of  doubt, 
search  for  the  treponema,  or  the  Wassermann  or  luetic  reaction  may 
be  employed. 

Tertiary  Syphilis  of  the  Mouth. — The  syphilides  of  the  secondary 
stage  arise  in,  and  are  confined  to,  the  mucous  and  dermal  structures; 
those  of  the  tertiary  stage  arise  in  the  deep  connective  tissues,  and 
are  frequently  associated  with  periosteum. 

Tertiary  lesions,  as  seen  by  the  dentist,  are  usually  in  the  form  of 
ulcers  of,  first,  the  soft  or  hard  palate,  and  of  the  tongue  or  lips.  In 
the  earlier  stages  hard,  nodular  formations  may  be  noted  as  ante- 
cedents to  the  ulcerations.  Chronic  periostitis  of  the  palatal  processes 
may  occur,  leading  to  the  formation  of  localized  thickenings.  In 
other  cases,  in  the  soft  palate,  upon  the  tongue,  or  in  the  hard  palate, 
localized  swellings  may  occur,  having  a -livid  red  appearance;  the 
overlying  mucous  membrane  breaks,  establishing  an  ulcer,  which 
may  perforate  the  soft  palate  and  destroy  a  portion  of  the  palatal 
process,  or  form  large  ulcers  on  the  tongue.  The  condition  is  one 
of  gumma.  These  lesions  appear  in  from  two  to  five  years  after  the 
secondary  manifestations. 

Tertiary  Lesions. — The  sight  and  hearing  may  be  affected,  the 
throat  diseased,  causing  loss  of  voice,  necrosis  of  the  bones  and  tissues 
of  the  nose  causing  deformity.  The  brain  or  spinal  cord  affected 
may  cause  paralysis,  locomotor  ataxia,  or  loss  of  reason.  These  are 
usually  the  result  of  failure  to  follow  treatment  to  a  conclusion. 

The  tongue  may  have  either  a  localized  or  widespread  parchment 
like  hyperplasia  of  the  mucous  membrane,  and  muscular  tissue  which 
may  cause  it  be  become  indented  by  the  teeth,  to  lose  its  papillae, 
and  become  dry  and  red.  Pedersen^  calls  attention  to  the  fact  that 
the  indentations  do  not  disappear  when  the  tongue  is  stretched, 
while  if  due  to  ordinary  debility  they  may  do  so. 

Although  there  is  much  doubt  as  to  the  degree  of  infectiveness  of 
these  tertiary  lesions,  precautions  as  to  sterilization  should  be  taken 
as  with  the  primary  and  secondary  lesions.    A  defined,  ragged  ulcer 

1  E.  Whitney:    Dental  Cosmos,  1911,  p.  524.  2  Dental  Cosmos,  1892. 

3  Ibid.,  1908,  p.  332. 


780  INFECTIONS  OF  AND  FROM  THE  MOUTH 

occupying  the  hard  or  soft  palate,  which  has  persisted  for  a  long 
time,  should  always  be  viewed  with  suspicion,  and  a  search  be  made 
for  other  evidences  of  syphilis. 

These  ulcerations  appearing  upon  the  side  of  the  tongue  may 
closely  simulate  epithelioma  of  that  organ.  The  confusion  is  increased 
if,  in  consequence  of  the  presence  of  jagged  teeth,  a  continuous 
irritation  is  excited.  Moreover,  leukoplakia  of  the  cheeks,  a  diag- 
nostic sign  of  incipient  epithelioma,  frequently  accompanies  tertiary 
syphilis. 

The  existence  of  tertiary  syphilis  is  of  great  clinical  importance  to 
the  dentist  in  that  a  condition  of  lessened  resistance  of  tissues  is 
established,  and  disease  processes  which  in  the  healthy  person  are 
comparatively  circumscribed,  in  the  syphilitic  run  a  riotous  course. 
A  septic  pericementitis  by  extension  may  involve  a  wide  area  of 
periosteum,  leading  to  extensive  maxillary  necrosis. 

Treatment. — The  treatment  of  syphilis  has  been  largely  by  the 
administration  of  mercury  and  potassium  iodid  for  a  long  period 
until  the  treponemata  shall  have  been  killed  out.  If  not  so  con- 
tinued the  tertiary  lesions  may  reappear  with  serious  results  The. 
latest  development  in  treatment  is  the  use  of  Ehrlich's  preparation 
of  arsenic,  dioxydiamedoarsenobenzol,  "606,"  or  "salvarsan,"  for 
which  positive  claims  as  a  prompt  cure  are  made. 

TUBERCULOSIS  OF  THE  MOUTH. 

The  bacillus  of  tuberculosis,  under  favorable  conditions,  develops 
in  the  tissues  of  the  mouth,  producing  its  characteristic  lesions. 
Finding  a  suitable  soil,  such  as  is  furnished  by  the  heredity  which 
predisposes  to  phthisis  pulmonalis,  the  bacillus  may  find  entrance 
to  the  deeper  tissues  from  the  mucous  membrane  of  the  mouth  and 
excite  tuberculosis  in  the  deep  structures,  the  bone,  etc.  A  number 
of  perforations  of  the  hard  palate  have  occurred.  According  to  Curtis 
these  are  usually  fatal.  What  part  is  played  by  local  oral  and  dental 
lesions  in  tuberculosis  of  distant  parts,  by  establishing  pathways 
for  the  entrance  of  the  bacilli  into  the  circulation,  is  at  present 
conjectural,  but  that  such  infections  occur  is  very  probable.  Lupus, 
a  skin  tuberculosis,  may  extend  to  the  mouth  producing  nodules. 

ACTINOMYCOSIS. 

The  condition  produced  by  the  development  of  the  ray-fungus,  the 
actinomycosis,  in  the  lower  jaw  and  cervical  regions  of  cattle  and 
swine — lump-jaw — is  not  unknown  in  human  beings.     It  may  be 


GENERAL  SEPTIC  DISEASES  OF  DENTAL  ORIGIN        781 

derived  by  chewing  straw  or  grass  in  which  the  ray-fungus  has 
produced  "rust." 

Miller^  gives  203  cases  reported  in  German  medical  literature 
between  1886  and  1891.  In  at  least  120  of  these  cases  the  point  of 
entrance  of  the  fungus  was  found  to  be  in  the  region  of  the  mouth  or 
throat.  Actinomycosis  threads  have  been  repeatedly  found  in  the 
saliva  and  in  carious  teeth,  and  notably  in  the  tonsils.  Whether  the 
path  of  entrance  to  deeper  structures  is  ever  through  carious  teeth 
is  undertermined,  but  certainly  lesions  or  wounds  about  the  mouth 
furnish  an  entrance.  Padgett  reports  a  case  of  alveolar  ulceration 
following  extraction,  which  proceeded  to  abscess  upon  the  face. 
Bacteriological  examination  showed  the  ray-fungus. 

The  disease  has  yielded  to  the  action  of  sulphate  of  copper,  -|- 
grain,  plus  iodid  of  potassium,  10  grains,  internally  four  times  a  day, 
together  with  local  irrigation  of  0.1  per  cent,  solution  of  copper 
sulphate.^ 

GONORRHEA. 

Cases  of  oral  infection  by  the  gonococcus  of  Neisser  have  been 
reported.  The  oral  mucous  membrane  and  the  gums  may  undergo 
intense  suppuration  with  its  accompaniment.  Fever  and  its  accom- 
paniments may  be  present.  The  eyes  are  very  subject  to  secondary 
infection  in  an  individual  suffering  from  gonorrheal  urethritis.  The 
hands  are  a  medium  of  transference.  Babes  may  be  directly  infected 
by  the  mother  during  birth,  and  blindness  often  results.  The  law 
now  requires  the  instillation  of  a  mild  solution  of  silver  nitrate  or 
other  antiseptic  as  advocated  by  Crede.  The  diagnosis  can  be  made 
by  microscopic  examination  of  the  bacteria.  Stein  claims  that 
endeavor  to  infect  the  nose  with  gonococci  failed  and  questions  oral 
infection  by  them.  (See  p.  677.)  Lederer  in  a  case  of  oral  infection 
in  a  patient  with  urethral  gonorrhea  foujid  it  by  microscopic  exami- 
nation to  be  a  case  of  Vincent's  angina,  which  see. 

GENERAL  SEPTIC  DISEASES  OF  DENTAL  ORIGIN. 

The  effect  of  the  existence  of  dental  diseases  upon  the  body  at 
large,  particularly  as  regards  secondary  infection,  is  a  matter  increas- 
ing in  importance  as  the  possibilities  of  their  connection  are  made 
out.  At  present  the  organisms  of  greatest  demonstrable  pathologi- 
cal interest  are  the  pyogenic  cocci.     The  almost  constant  presence 

1  Dental  Cosmos,  1891.  2  Brophy:    Dental  Cosmos,  1908,  p.  78. 


782  INFECTIONS  OF  AND  FROM   THE  MOUTH 

of  these  organisms  in  the  mouth,  carried  thence  into  the  pharynx, 
posterior  nares,  larynx,  lungs,  and  stomach,  furnishes  the  reason  for 
the  pyogenic  and  phlegmonous  inflammations  which  occur  in  these 
organs.  The  diplococcus  of  pneumonia,  a  frequent  organism,  but 
waits  a  favorable  opportunity  to  establish  high  inflammations  and 
fibrinous  exudations  in  the  lungs,  and  possibly  in  other  structures. 

The  most  important  clinical  associations  of  dental  with  general 
infections  are  diseases  of  the  pericementum.  The  pulps  of  teeth, 
having  no  lymphatics,  do  not  appear  to  take  up  and  transmit  the 
products  of  the  action  of  septic  organisms;  but  while  the  evidences 
of  such  absorption,  involvement  of  the  neighboring  lymphatics,  are 
not  present,  it  must  be  remembered  that  the  veins  may  transmit 
the  poison,  and,  in  addition,  may  perhaps  convey  organisms  from  a 
diseased  but  still  vital  pulp  to  distant  parts.  When,  however,  the 
pulp  is  dead  and  the  pericementum  is  invaded,  there  is  no  doubt  of 
general  infection  from  this  local  source.  More  or  less  septic  intoxica^ 
tion  is  a  common  attendant  upon  severe  septic  apical  pericementitis, 
and  septicemia  accompanied  by  inflammation  of  the  neighboring 
lymphatic  glands  is  of  sufficient  frequency  to  emphasize  the  need 
of  the  vigorous  antiseptic  treatment  recommended  in  all  of  these 
cases. 

Pyemia  is  far  more  uncommon.^  Pyogenic  organisms,  gaining 
access  to  the  blood  current  from  the  local  source  of  infection,  establish 
suppuration  in  distant  parts;  in  other  parts  of  the  bone,  or  in  other 
bones  (osteomyelitis),  in  the  lungs,  meninges,  and  substance  of  the 
brain.  One  case^  has  been  reported  where  abscess  of  a  toe,  ear,  and 
forearm  ceased,  and  recovery  took  place  after  treatment  and  filling 
of  septic  root  canals.  Several  cases  are  tabulated  by  the  same  author 
in  which  extensive  necrosis  and  death  resulted  from  pyemic  infec- 
tion from  septic  pericementitis.  Some  of  these  cases  recorded  were 
associated  with  acute,  some  with  chronic,  septic  pericementitis. 

In  addition  to  the  usual  pyogenic  cocci.  Miller  has  isolated  several 
forms  of  cocci,  bacilli,  and.  spirilla,  forming  products  which,  if  injected 
into  the  circulation  of  animals,  cause  death  from  septicemia  in  from 
hours  to  days.  As  many  of  these  forms  may  be  brought  into  rela- 
tion with  deep  parts  by  the  anatomical  conditions  created  by  pulp 
death,  the  possibilities  of  many  types  of  infection  uia  pulpless  teeth 
are  evident. 

The  possibilities  of  local  as  well  as  general  infections  through  the 
conditions  established  in  the  several  forms  of  pyorrhea  alveolaris 
should  not  be  forgotten.    (See  pp.  438,  603,  605,  631,  742,  787.) 

1  Miller:    Dental  Cosmos,  1891.  ^  Ibid. 


LEUKOPLAKIA  BUCCALIS  783 

The  pockets  formed  by  the  soft  tissues  overhanging  lower  third 
molars  whose  eruption  is  impeded  invite  the  passage  of  septic  organ- 
isms to  deep  parts.  Local  pyogenic  infections  are  common  in  these 
cases,  and  may  extend  into  the  pharynx  and  the  submaxillary  tissues, 
as  in  Ludwig's  angina. 

HERPES  LABIALIS   (HERPES  SIMPLEX). 

This  consists  of  a  vesicular  eruption  upon  the  lip,  tongue,  mouth, 
cheeks,  or  allse  of  the  nose.  The  vesicles  are  filled  with  a  clear  fluid 
which  soon  discharges.  An  excoriation  is  left  often  covered  by  a 
light  crust,  which  is  never  followed  by  a  scar.  The  condition  may 
cause  little  pain  or  considerable  burning  and  itching.  It  may  accom- 
pany colds,  fevers,  exposure  to  heat,  draughts,  and  gastric  disorders. 
It  follows  either  a  direct  irritation  of  the  nerves,  as  after  the  use  of 
rubber  dam  or  other  dental  operations  in  susceptible  persons,  or  may 
be  of  reflex  origin;  in  either  case  localized  peripheral  neuritis  being 
the  initial  lesion. ^  There  is  some  reason  to  believe  that  infection 
plays  a  part  in  its  production.  As  a  preventive  it  is  w^ell  to  lubricate 
the  lips  with  glycerin  and  rose  water  or  with  cold  cream  when  much 
stretching  or  other  irritation  is  necessary. 

HERPES  ZOSTER. 

This  is  a  probably  infectious  disease,  almost  invariably  mono- 
lateral,  associated  with  a  neuritis  usually  of  a  spinal  ganglion  or  with 
a  peripheral  neuritis,  which  produces,  first,  a  hyperesthesia  of  the 
integument,  macules,  and  later  vesicular  eruptions  not  usually 
beginning  on  a  mucous  surface.  They  appear  in  groups  and  may 
coalesce,  forming  patches.  Desiccation  forms  a  crust;  pus  may 
form. 

The  interest  to  dentists  lies  in  the  fact  that  in  zoster  of  the  head 
exfoliation  of  the  teeth  is  said  to  be  associated  in  rare  cases.^ 

LEUKOPLAKIA  BUCCALIS.^  - 

Upon  the  inner  surface  of  the  cheeks  or  lips,  and  upon  portions  of 
the  gum  and  the  dorsum  and  edges  of  the  tongue,  may  appear  sharply 
outlined,  dull,  whitish,  slate-colored  or  silver-whitish  points,  disks, 
streaks,  bands,  ribbons,  or  patches  of  irregular  shape,  either  flattened 
or  slightly  elevated,  above  the  general  level  of  the  mucous  surface. 
They  may  crack  or  fissure,  and  inflammation  of  the  derma  and  pain 

1  Hyde  and  Montgomery:    Diseases  of  the  Skin.  -  Ibid.  ^  Ibid. 


784  INFECTIONS  OF  AND  FROM  THE  MOUTH 

result.  Ordinarily  they  are  simply  rough  and  without  much  dis- 
comfort. It  occurs  almost  exclusively  in  males.  They  differ  from 
the  mucous  patches  of  syphilis  in  that  the  latter  are  soft  and  tend  to 
ulcerate,  and,  while  they  may  accompany  syphilis,  may  occur  in  its 
absence  or  of  any  history  of  it. 

They  simulate  the  keratosis  of  lichen  planus,  which  should  also 
appear  as  papules  upon  other  parts  of  the  body. 

Apart  from  syphilis,  it  is  due  to  irritation  such  as  that  from 
tobacco  or  rough  teeth,  and  with  syphilis,  tobacco,  and  rough  teeth 
may  be  additional  excitants. 

R.  H.  Ivy  reports  three  cases  with  tendency  to  epitheliomatous 
degeneration,  all  without  history  of  syphilis,  and  in  two  of  which 
the  Wassermann  reaction  was  negative.^ 

The  use  of  alcohol  and  spices  are  also  a  cause. 

The  pellicle  is  closely  adherent,  and  consists  of  an  hypertrophied 
and  hyperkeratinized  epithelium,  with  more  or  less  inflammatory 
infiltration  of  the  derma  and  with  partial  obliteration  of  the  papillse. 

The  chief  danger  in  the  disease  is  the  tendency  to  epithelioma, 
some  authors  estimating  30  per  cent.,  especially  in  the  cases  in  which 
exfoliation  and  ulceration  occur.  Some  fourteen  years  ago  a  male 
patient  presented  with  a  leukoplakia  in  which  there  was  a  constant 
desquamation  as  though  very  hot  liquids  had  been  used.  Medical 
treatment  was  given,  tobacco  and  liquor  were  largely  avoided,  but 
after  about  twelve  years,  epithelioma  involving  a  jaw  operation 
occurred. 

The  removal  of  the  pellicles  by  suitable  caustics,  galvanocautery, 
or  bur,  and  radiotherapy,  the  use  of  soothing  mouth  washes,  together 
with  a  hygienic  regimen,  and  the  avoidance  of  irritants  like  tobacco, 
alcohol,  spiced,  hot,  or  iced  foods,  is  the  usual  treatment  to  avoid 
epithelioma.  The  diagnosis  lies  clearly  within  the  province  of  the 
dentist  who  may  note  it  before  the  patient.  The  treatment  is 
usually  conducted  by  the  physician,  and  is  often  unsatisfactory  as 
to  permanent  cure.  Cases  with  syphilitic  history,  of  course,  require 
antisyphilitic  treatment. 

Leukoplakia  has  been  also  called  buccal  psoriasis,  but  psoriasis 
does  not  affect  mucous  surfaces,  hence  it  is  a  misnomer. 

LICHEN  PLANUS. 

This  condition,  which  may  simulate  leukoplakia,^  is  characterized 
by  an  eruption  consisting  of  glistening  flat-topped  polygonal  papules 

1  New  York  Medical  Journal,  October,  1912,  p.  1187. 

2  Ibid.,  April  13,  1912. 


PHOSPHOR  NECROSIS  785 

with  tendency  to  form  irregularly  arranged  groups.  On  the  mucous 
surface  they  appear  as  whitish  macules,  striae,  or  flat  papules  on  both 
sides  of  the  tongue  at  the  points  in  contact  with  the  molar  teeth. 

They  are  the  result  of  an  arterial  or  venous  hyperemia  of  the 
papillee  of  the  corium,  a  secondary  thickening  of  the  lower  part  of 
the  rete,  and  a  tertiary  flattening  of  the  papule  by  pressure. 

A  proliferation  of  cells  in  the  granular  layer  and  a  deposit  of 
keratohyalin  in  whitish  spots  occur.  This  causes  a  similarity  to 
leukoplakia.  It  usually  occurs  in  the  nervously  exhausted,  though 
many  patients  may  have  a  fair  degree  of  body  nutrition  while  yet 
nervously  exhausted. 

PHOSPHOR  NECROSIS. 

This  disease  is  a  more  or  less  extensive  necrosis  of  the  maxillse  due 
to  the  entrance  of  phosphorus  or  its  fumes  into  contact  with  the 
periosteum  or  pericementum  of  a  tooth. 

It  was  formerly  frequent  in  match  factories,  when  white  phosphorus 
was  used,  though  now  less  when  the  red  is  employed,  but  has  occurred 
through  the  chewing  of  match  heads,  and  a  case  has  been  reported 
in  which  a  half  grain  taken  in  three  days  caused  it.^ 

As  it  does  not  ordinarily  occur  in  the  mouths  of  those  having 
sound  teeth,  it  is  generally  regarded  as  of  local  origin,  the  phosphorus 
gaining  entrance  either  through  the  pulp  canal  of  a  tooth,  or,  possibly, 
through  some  point  of  injury  external  to  the  tooth. 

Abscesses  containing  offensive  pus  cause  great  swelling  and  exces- 
sive salivation,  and  may  cause  several  fistulse,  while  the  swallowing 
of  the  discharge  causes  general  toxic  disturbance,  and  infection  such 
as  pneumonia  or  cerebrospinal  meningitis  may  have  rapid  effect. 

The  periosteum  remains  unaffected  as  to  its  vitality,  while  the 
bone  proper  undergoes  osteoporous  necrosis,  becoming  like  rotten 
sponge.  As  the  sequestrum  is  separated,  there  is  a  tendency  to 
formation  of  new  bone  by  the  periosteum.  The  necrosis  of  bone  may 
be  very  extensive,  involving  in  the  lower  jaw  the  entire  horizontal 
portion,  while  the  ramus  may  remain  unaffected.  In  the  lower  jaw, 
after  exfoliation,  the  bone  may  be  almost  entirely  restored  to  an 
amount  nearing  fair  comparison  with  the  ordinary  edentulous 
mouth,  while  in  the  upper  jaw  no  repair  occurs.  This  new  bone  may 
undergo  atrophy  if  not  put  to  work  by  artiflcial  teeth.^  As  a  pro- 
phylactic sodium  bicarbonate  solutions  are  recommended  by  Arnone.^ 

1  Arnone:    Dental  Cosmos,  1910,  p.  425. 

-  For  consideration  of  treatment  the  reader  is  referred  to  Garretson's  System  of 
Oral  Surgery,  sixth  edition,  and  other  writings  upon  the  subject. 
3  Dental  Cosmos,  1909. 
50 


786 


INFECTIONS  OF  AND  FROM  THE  MOUTH 


SCORBUTUS. 

This  is  scurvy  as  described  on  pages  215,  649,  684,  and  below. 


PURPURA  HEMORRHAGICA. 

This  is  the  appearance  of  small  purplish  spots  beneath  the  skin 
and  mucous  membrane,  and  is  dependent  upon  infection  and  toxic 
conditions, 

Brown,^  following  Schamberg,  presents  the  following  clear  differ- 
ential symptoms : 


Scorbutus. 

1.  Occurs  in  those  subjects  due  to  lack 

of  vegetable  food  and  to  bad  hy- 
giene. 

2.  Definite  antecedent  symptoms,  weak- 

ness, impaired  circulation,  etc. 

3.  Onset  slow. 

4.  Gums  spongy,  swollen,  and  bleeding; 

teeth  loose. 

5.  Severe  muscular  pain. 

6.  Brawny  infiltration  of  lower  extremi- 

ties. 

7.  Hemorrhages     from     mucous     mem- 

branes, not  profuse,  as  a  rule. 


Purpura  Hemorrhagica. 

1.  No  such  etiological  relationship, 

2.  Antecedent  signs  shght  or  absent. 

3.  Onset  sudden. 

4.  Gums  often  bleeding,  but  not  swollen. 

5.  Less  marked, 

6.  Not  present, 

7.  Hemorrhages    from    mucous    mem- 

branes so  severe  as  to  sometimes 
prove  fatal. 


LEPROSY. 

During  the  progress  of  leprosy,  an  infective  disease,  characteristic 
nodules  and  ulcers  appear  about  the  oral  structures.  As  many  parts 
of  the  head  are  affected  in  like  manner,  these  are  but  symptoms  of 
the  progress  of  the  effects  of  the  Bacillus  lepra,^ 


ANGINA. 

Angina  is  usually  defined  as  a  sense  of  choking  or  suffocation, 
a  symptom  which  accompanies  inflammatory  affections  of  the 
pharynx  as  well  as  the  paroxysmal  neuralgic  affection  of  the  heart 
known  as  angina  pectoris. 

Angina  Simplex. — This  is  inflammation  of  the  pharynx,  with,  of 
course,  more  or  less  swelling  and  infiltration  of  exudate.  Swallowing 
may  be  difficult.  Local  depletion  and  sedative  washes,  with  general 
derivation,  are  indicated.  If  chronic,  stimulant  washes  are  useful 
combined  with  general  tonic  treatment, 

1  Dental  Cosmos,  1911,  p.  296. 

^  For  an  exhaustive  article  see  Oliver,  Dental  Cosmos,  1908. 


ANGINA  787 

Ludwig's  Angina. — In  1836  Ludwig  described  a  disease  which  is 
considered  to  be  an  infectious  celluhtis  in  the  submaxillary  region, 
which  may  extend  deeply  into  the  tissues  of  the  neck.  The  infection 
is  thought  to  be  due  to  the  Streptococcus  pyogenes  or  bacillus  of 
malignant  edema,  though  the  Staphylococci  and  Diplococcus  pneu- 
monise  are  found,  and  probably  enter  the  cellular  tissue  of  the 
submaxillary  region  and  neck  through  the  oral  or  pharyngeal  mucous 
membrane  or  a  wound.  An  apical  abscess,  also,  the  repeated  impac- 
tion of  food  into  the  peridental  region,  especially  about  a  third 
molar,  and  its  fermentation  has  caused  a  deep  infection  resulting  in 
this  disease.    The  patient  has  lassitude,  chilliness,  and  fever. 

A  hard  swelling  appears  beneath  the  mandible  after  several  days, 
and  extends  toward  the  neck  and  under  the  tongue.  There  is  mus- 
cular rigidity  and  the  head  is  inclined  in  one  direction.  The  skin  is 
not  much  reddened. 

Later  edema  is  marked  and  may  extend  upward  toward  the 
parotid  gland  or  the  glottis.  Breathing  and  swallowing  are  rendered 
difficult  by  oral  and  pharyngeal  swellings.  There  are  the  usual  oral 
symptoms  of  inflammation.  Upon  incision  the  connective  tissues 
are  found  to  be  sloughing,  grayish  black  in  color,  and  may  ooze  pus. 

The  board-like  hardness  of  the  floor  of  the  mouth  and  the  marked 
dyspnea  are  constant  features. 

The  spread  of  the  infection  being  by  continuity  of  cellular  spaces, 
the  glands  are  much  enlarged. 

A  large  abscess  may  form  and  discharge.  Pneumonia,  septicemia, 
and  pyemia  are  complications  to  be  feared  as  the  result  of  spreading 
infection.  Incisions  for  drainage  and  antisepsis  are  usually  con- 
joined with  systemic  treatment,  but  as  the  case  is  often  of  dental 
origin  the  cause  should  be  removed. 

Vincent's  Angina. — This  is  an  edematous  tonsillitis,  which  may 
affect  also  the  mucous  membrane  of  the  mouth  and  pharynx,  fol- 
lowed by  the  formation  of  a  pseudomembrane  as  in  diphtheria,  later 
ulceration  and  hemorrhage  may  appear.  There  are  the  usual  accom- 
paniments of  inflammation  in  this  locality,  together  with  fever  and 
sometimes  rigors.  It  usually  lasts  about  two  weeks.  It  also  occurs 
about  the  gums  without  necessarily  affecting  the  pharynx,  and  here 
may  last  much  longer. 

The  differential  diagnosis  from  diphtheria  and  syphilis  is  made  by 
microscopic  examination.  Vincent's  bacilli,  spindle-shaped,  pointed 
at  extremities,  and  6  to  10/x  in  length,  are  usually  associated  with  a 
long  thin  spirillum.      (See  Fig.  611.) 

They  take  several  stains,  but  not  the  Gram.  In  diphtheria, 
Loeffler's  bacilli,  and  in  syphilis  the  treponema  pallidum  would  be 


788  INFECTIONS  OF  AND  FROM  THE  MOUTH 

found.       Tuberculosis,  gonorrhea,   stomatitis,   and   pyorrhea  must 
also  be  differentiated.     (Lederer.) 

In  the  treatment  mercuric  chlorid  1  to  10,000  in  4  per  cent,  boric 
acid  solution,  and  especially  salvarsan,  10  per  cent,  in  sesame  oil, 
suspended  by  the  aid  of  lodipin  (Merck)  is  recommended  for  injec- 
tion into  the  pockets  or  applied  to  the  gum,  are  highly  recommended 
by  Lederer.  The  writer  has  cured  a  number  of  cases  of  this  type 
by  the  use  of  mercuric  chlorid,  1  grain  in  each  four  ounces  of  H2O2. 
A  microscopic  examination  was  not  made.^  Vaughan  recommends 
silver  nitrate,  4  to  8  per  cent.,  Lugol's  solution,  chromic  acid,  10  per 
cent.,  zinc  chlorid,  2  per  cent.,  and  Argyrol  full  strength,  also  a  light 
diet  and  cathartics. 

DENTAL  STERILIZATION. 

It  must  ever  be  borne  in  mind  that  the  dental  operator  constantly 
works  in  a  field  of  infection,  and  unless  extraordinary  precautions  be 
taken  every  instrument  which  touches  this  field — the  fingers  of  the 
operator,  his  mirrors,  glasses,  napkins,  rubber  dam,  rubber  dam 
clamps — becomes  immediately  infected  as  soon  as  it  is  brought  in 
contact  with  the  mouth  of  the  patient.  The  likelihood  of  infection 
varies  with  the  patient  and  the  particular  instruments;  mouth 
mirrors,  rubber  dam  clamps,  scalers,  and  all  instruments  used  in  the 
treatment  of  pulp  canals  are  likely  to  become  more  promptly  and 
extensively  infected  than  other  instruments.  Again,  the  forms  of 
the  instruments  determine  whether  or  not  increased  opportunity  is 
given  for  the  retention  of  infective  material.  The  fingers  of  the 
operator  may  be  the  medium  through  which  infective  material  is 
transferred  from  one  patient  to  another.  Infection  may  be  carried 
from  superficial  areas  of  the  mucous  membrane  of  the  mouth,  from 
the  enamel  and  the  saliva,  into  deeper  structures,  where  conditions 
are  favorable  for  the  development  of  sepsis. 

The  scheme  for  dental  sterilization,  therefore,  includes  the  steriliza- 
tion of  the  operator,  instruments,  apparatus,  appliances,  etc.,  used 
in  operations,  and  the  sterilization  of  the  field  of  operation  prior  to 
operating. 

The  Operator. — Extreme  personal  cleanliness  upon  the  part  of  an 
operator  is  clearly  the  first  step  in  asepsis.  The  best  class  of  dentists 
are  exceedingly  neat  as  regards  personal  habits ;  daily  bathing,  care  of 
the  nails  and  of  the  skin,  and  immaculate  linen  form  as  much  a  part 
of  the  day's  labor  as  dental  operations  per  se.     The  virtues  of  soap 

1  For  an  exhaustive  article  see  Vaughan,  Dental  Cosmos,  June,  1912. 


DENTAL  STERILIZATION  789 

and  water,  wherever  they  may  be  applied,  are  regarded  as  a  very 
important  item  in  preventing  infection. 

Linen  which  has  been  boiled  prior  to  wearing  may  be  regarded  as 
safely  sterile;  so  that  the  matter  of  personal  sterilization  relates  to  the 
hands,  particularly  to  the  finger-nails.  The  space  under  the  nails  is 
a  favorable  habitat  for  many  organisms,  notably  the  pyogenic  cocci, 
the  staphylococcus  pyogenes  aureus  being  commonly  present  in  this 
situation. 

It  has  always  been  advised  that  the  finger-nails  be  trimmed  short, 
and  be  made  smooth  to  avoid  mechanical  injury  to  the  soft  tissues 
of  the  patient.  Since  the  advent  of  aseptic  and  antiseptic  surgery 
these  precautions  have  an  additional  significance;  nails  kept  short 
and  smooth  may  be  more  readily  cleansed  than  if  long  and  ill-kept. 
The  nails  should  be  cut  so  that  they  nowhere  project  beyond  the  tips 
of  the  fingers.  Their  mechanical  cleansing  should  be  done  with 
smooth  instruments,  not  sharp  knife-blades;  the  latter  produce 
rough  surfaces,  which  furnish  spaces  for  lodgement  of  bacteria.  There 
is  but  one  effective  method  of  washing  beneath  the  nails;  it  is  that 
followed  by  the  general  surgeon.  After  dipping  the  soap  in  water  as 
hot  as  can  be  borne  by  the  hands,  all  of  the  finger-nails  should  be 
made  to  scrape  the  soap  until  the  spaces  under  the  nails  are  filled 
with  soap.  After  this  coarse  hand-brushes  are  used  to  scour  every 
part  of  the  hands  with  soap  and  water  as  hot  as  can  be  borne.  Special 
nail-brushes  are  next  used  to  scrub  beneath  the  nails,  driving  out 
piecemeal  the  soap  masses  there.  The  general  surgeon  continues  the 
scrubbing  until  the  nails  are  scrupulously  clean.  The  soap  usually 
used  is  Castile,  or  soap  made  from  palm  oil,  etc.,  but  antiseptic 
soaps,  such  as  ethereal  soaps,  may  be  substituted  with  advantage. 
Tincture  of  green  soap  is  effective  (see  below). 

Sterilization  of  the  cleansed  hands  is  insured  by  immersing  them 
for  five  minutes  in  antiseptic  solutions,  such  as  50  per  cent,  alcohol. 
The  hands  should  be  sterilized  after  treating  each  patient;  rubbing 
the  hands  with  a  paste  of  mustard,  flour,  and  water  for  three  minutes 
and  washing  off  with  sterilized  water  is  effective.  (Nancrede.)  If 
the  patient  dismissed  has  possessed  an  unusually  septic  mouth,  or  has 
been  a  syphilitic,  for  example,  the  time  for  hand  cleansing  and  ster- 
ilization is  to  be  prolonged;  if  syphilitic,  every  instrument  used  is 
transferred  to  separate  vessels  containing  antiseptic  solutions  or 
boiled,  and  the  hands  are  viewed  as  highly  infected ;  they  are  scrubbed 
with  mercuric  chlorid  solutions  to  prevent  personal  infection  or  the 
carriage  of  infection.  Chancres  have  from  time  to  time  appeared 
upon  the  fingers  of  dentists  as  well  as  physicians.  In  a  known 
syphilitic  case  one  might  use  the  rubber  gloves  worn  by  surgeons,  at 
any  rate  all  abrasions  should  be  covered  with  collodion. 


790  INFECTIONS  OF  AND  FROM  THE  MOUTH 

Sterilization  of  Apparatus. — The  scrupulous  cleanliness  of  the  oper- 
ating chair,  of  which  the  head-rest  should  receive  frequent  changes  of 
boiled  linen  coverings,  the  metallic  parts  should  be  rubbed,  and  general 
covering  cleansed; the  cleansing,  polishing,  and  sterilizing  of  cuspidors; 
the  changing  of  paper  coverings  upon  instrument  tables,  etc.,  are  part 
of  the  general  scheme  of  sterilization.  The  floor  of  the  operating 
room  also  requires  attention;  instead  of  being  covered  with  carpet,  it 
is  preferable  to  have  it  made  of  parquetry  material  or  cement,  over 
which  rugs  are  laid,  which  may  be  removed  from  the  room  for 
cleansing;  the  floor  proper  being  scrubbed. 

Napkins  used  about  the  mouth  are  certain  to  become  infected,  so- 
that  their  boiling  should  be  prolonged  at  least  fifteen  minutes.  For 
many  operations  it  is  preferable  to  substitute  strips  of  muslin  for 
linen  napkins,  which  after  being  used  may  be  thrown  away. 

If  a  hydraulic  saliva  ejector  be  used,  the  glass  mouth  tubes  should 
be  changed  for  each  person,  a  sterilized  tube  being  substituted 
directly  before  its  use  is  required.  A  number  of  these  tubes  should 
be  in  use,  and  may  be  sterilized  after  washing  by  placing  them  in  a 
50  per  cent,  solution  of  listerine  or  a  formaldehyd  solution  for  a  few 
hours.  Tumblers  and  mouth  mirrors  may  be  sterilized  in  like 
manner.  The  cloudiness  of  saliva  tubes  is  produced  by  the  forma- 
tion of  salivary  calculus,  and  may  be  removed  by  the  use  of  acidulated 
water.  ^ 

At  the  close  of  each  day  a  large  cup  should  be  filled  with  an  anti- 
septic solution,  which  is  to  be  drawn  through  the  tubing  of  the  ejector 
to  keep  it  in  a  reasonably  aseptic  condition. 

^Rubber  dam  may  be  sterilized  by  boiling  water,  but  it  is  more 
safe  and  cleanly  to  use  a  new  piece  for  each  patient.  It  should  be 
washed  and  then  dusted  with  borated  talcum  powder. 

The  water  used  for  douching  cavities  should  be  boiled  previous  to 
placing  in  the  warmer,  and  should  have  a  little  pleasant  antiseptic 
added  to  it. 

Nancrede^  states  that  all  pyogenic  cocci,  and  even  anthrax  spores, 
are  killed  by  boiling  instruments  for  two  minutes  in  a  1  per  cent, 
solution  of  sodium  carbonate,  which  also  prevents  rusting. 

Mouth  mirrors  and  other  instruments  which  can  be  wet  may  be 
placed  for  one-half  hour  or  longer  in  a  covered  jar  containing  20  per 
cent,  formaldehyd,  to  which  borax  has  been  added  to  saturation. 
Rusting  is  prevented  by  borax  (Williams). 

Broaches,  trephines,  and  other  small  points  requiring  to  be  kept 
sterile  may  be  placed  in  a  bottle  such  as  are  sold  containing  gold 
cylinders,  and  kept  wet  with  any  essential  oil  or  carbolic  acid. 

1  Thornton:    Dental  Review,  1903.  ^  Park's  Surgery  by  American  Authors. 


DENTAL  STERILIZATION  791 

G.  Zederbaum^  suggests  sticking  the  shanks  in  the  cork;  when  to 
be  used  the  cork  is  to  be  transferred  to  another  bottle  of  like  size 
containing  alcohol  and  shaken  to  remove  the  antiseptic.  They  may 
then  be  washed  in  sterilized  water. 

Extracting  forceps  require  careful  mechanical  cleansing  and  pro- 
longed boiling  after  each  use,  for  perhaps  more  cases  of  infection, 
and  of  many  kinds,  have  resulted  from  unclean  forceps  than  from 
all  other  causes  combined. 

Instruments,  such  as  hand-pieces,  which  cannot  be  conveniently 
wet  may  be  wiped  off  with  alcohol  and  then  subjected  for  thirty 
minutes  to  formaldehyd  gas,  any  closed  vessel  may  have  cotton  rolls 
saturated  with  liquid  formaldehyd  placed  therein.  Enough  gas  is 
given  off  to  disinfect.  Lacking  a  special  apparatus  an  aluminum 
omelet  pan  with  the  handle  filed  off  makes  a  convenient  and  not 
unsightly  sterilizer.  If  desired,  all  the  instruments  may  be  so  steril- 
ized. These  methods  involve  the  employment  of  several  instruments 
of  each  kind,  an  economy  of  time  in  any  event.  The  entire  instru- 
ment case  may  be  disinfected  by  placing  a  formalin  tablet  in  each 
drawer  (Miller). 

Sterilizing  the  Field  of  Operation.  A  good  method  is  to  forcibly 
spray  the  mouth  with  a  1  to  3  per  cent,  solution  of  hydrogen  dioxid, 
in  order  to  force  infective  material  from  about  the  teeth.  The  other 
solutions,  as  a  solution  of  potassium  permanganate  or  mercuric 
cholorid  or  alcohol  may  then  be  used.  This  spraying  or  washing 
should  be  somewhat  prolonged  when  the  mucous  membrane  is  likely . 
to  be  injured,  as  in  extractions  which  often  result  in  infection  from 
the  patient's  own  secretions.  Many  operators  keep  a  stock  of  inex- 
pensive toothbrushes  for  such  cases,  which  are  thrown  away  after  the 
patient  has  used  them,  who  is  directed  to  scrub  the  teeth  well  with 
the  brush  and  the  antiseptic  solution. 

For  very  thorough  disinfection  thoroughly  cleanse  the  teeth  and 
use  the  antiseptic  between  them  upon  floss  silk.  For  surgical  work 
or  etherization  very  active  work  should  be  done.  Wadsworth,^  in 
an  investigation  of  mouth  washes  and  their  action  on  pneumococci, 
found  but  little  value  in  the  ordinary  wash  or  even  solutions  of 
formalin,  lysol,  or  H2O2.     He  found  that 

I^— Alcohol 30  parts 

Water 70  parts 

Glycerin  and  salt,  a  small  quantity  added. 

was  very  effective  in  destroying  the  bacteria. 

1  Dental  Cosmos,  1907.  2  Ibid. 


792  INFECTIONS  OF  AND  FROM  THE  MOUTH 

In  a  series  of  tests  upon  the  devitalizing  power  of  germicides  for 
streptococcus,  gonococcus,  pneumococcus,  and  Bacillus  typhosus, 
Post  and  NicolP  found  tincture  of  "green  soap"  (a  brownish  liquid 
composed  chiefly  of  alcohol  and  caustic  potash),  alcohol  in  solutions 
above  50  per  cent.,  silver  nitrate  solution  from  1  to  1000  to  stronger, 
tincture  of  iodin,  Senn's  solution  (iodin  1,  potassium  iodid  1,  water 
100  and  even  400),  phenol,  5  per  cent.,  and  chloroform  were  effective 
in  one  minute. 

Potassium  chlorate,  mercuric  chlorid,  1  to  500,  failed  in  ten  minutes. 
Boric  acid  failed  in  two  hours.  As  some  of  these  germicides  are  for 
the  mouth  and  some  for  the  hands  the  information  is  of  great  practical 
value.  Perhaps  the  best  method  of  sterilizing  gums  for  injections 
or  gum  margins  for  work  is  to  spray  off  any  accumulation  and  apply 
tincture  of  iodin  for  a  few  minutes. 

The  routine  practice  of  scaling  and  polishing  the  teeth  and  pre- 
scribing an  antiseptic  mouth  wash  prior  to  the  commencement  of  a 
series  of  sittings  is  to  be  highly  commended. 

In  scaling  the  writer  uses  antiseptic  washes  freely  during  the 
entire  operation. 

If  ulcerations  or  inflammatory  conditions  exist,  the  sterilization 
is  to  be  prolonged.  If  a  suspicion  of  syphilis  exist,  not  only  should 
the  mouth  be  freely  washed  with  strong  antiseptics,  but  special 
instruments  should  be  used,  preferably  an  old  set,  kept  sterilized  and 
used  only  in  special  cases. 

A  deep  infection  may  usually  be  prevented  during  the  treatment 
of  pyorrhea  alveolaris  and  pulp  gangrene  by  attention  to  the  ster- 
ilization of  the  infected  tract  before  beginning  work  upon  the  parts 
or  during  its  progress.  These  methods  have  been  indicated  in  the 
discussion  of  these  subjects. 

1  Spence:    Dental  Cosmos,  1911,  p.  548. 


INDEX. 


Abnormal  food  supply,  28 

nerve  supply,  29 

physical  conditions,  29 

waste  removal,  29 
Abrasion,  300 

acids  in,  306 

in  animals,  308 

of  calculus,  306 

degrees  of,  301 

during  sleep,  301,  311 

effects  of,  307 

from  clasp,  306 

gritty  powders  as  cause  of,  305 

labial  and  approximal,  303 

lingual,  307 

occlusal,  300 

pulp  hyperemia  in,  477 

relation  to  caries  in,  303,  307 

tooth-brush  in,  306 

treatment  of,  309 
Abscess,  apical,  acute,  586 
causes  of,  586 
clinical  history  of,  593 
diagnosis  of,  595 
extraction  in,  603 
guards  in,  599 
pathology  of,  588 
scar  threatened  in,  606 
stages  of  pus  formation  in, 

589 
symptoms  of,  588 
systematic     stopping     in, 

613 
systemic  complication  in, 

604,  607,  630,  643 
treatment  of,  598 
varieties  of,  592,  597 
chronic,  609 

blind,  631,  642 
necrosis  from,  635 
scar  from,  534 
symptoms  of,  617 
in  temporary  teeth,  638 
treatment  of,  618 
with  fistula,  614 
without  fistula,  609 

around  third  molar,  234 

fistula  in,  134,  614 

perforation  of  bone  in,  601,  614 

pericemental,  745 


Abscess,  pointing  in,  134,  604 

of  pulp,  497 

pus  in,  134 

syringe,  619 
Absence  of  teeth,  275 
Absorbent  organ,  217 
Acacia,  use  of,  207 
Accidents  to  teeth,  671 
Acetanilid  as  cause  of  hemorrhage,  120 

use  of,  400,  491,  605 
Acidity,  hyper-,  98,  102,  307,  359,  415, 

740,  741 
Acidosis,  acids  in,  93 
Aconite,  tincture  of,  124,  234,  476 
Aconitin,  use  of,  234 
Actinomycosis  of  mouth,  780 
Aerogenic  bacteria,  45 
Adenoids  in  mouth  breathing,  224,  228 
Adrenalin,  use  of,  403,  517 
Age  as  predisposition,  31 
Agenesia  of  enamel,  260 
Agglutination,  61 
Air  warm,  use  of,  401 
Albumin,  fermentation  of,  47 
Albuminuria,  112 
Alcohol,  injection  of,  765 

use   of,    150,    401,    423,    789,    791, 
992 
Alexins,  54 

Aloin  compound,  use  of,  689 
Alopecia,  from  dental  disease,  763 
Alteration,  definition  of,  21 
Alum,  use  of,  483,  490,  491,  612 
Alveolar  process,  fracture  of,  672 
Alveolitis,  postextraction,  603,  633,  672 
Amalgam,  copper,  use  of,  430,  561 

facing,  527 
Amboceptors,  61 
Ameba  of  dysentery,  38 

properties  of,  18 

of  pyorrhea,  714 
Ameloblasts,  160 
Ammonia,  use  of,  423,  642 
Ammonol,  use  of,  400 
Amputation  of  roots,  619,  623,  727 
Amyl  nitrite,  use  of,  519 
Anemia,  114,  116 
Anesthesia  of  apical  tissue,  520 

conductive,  407,  482,  520 

diplcsic,  408 

general,  use  of,  398,  515 

mucous,  407,  482 

(793) 


794 


INDEX 


Anesthesia  of  nerve  trunk,  407 

by  pressure.     See  Pressure. 

of  pulp,  404,  407,  515 

reflex,  409 
Angina,  Ludwig's,  235,  787 

simplex,  786 

Vincent's,  675,  681,  787 
Angle,  classification  of  malocclusion  by, 

223 
Ankylosis,  dental,  654 
Anomalies  of  teeth.  See  Malformations. 
Antikamnia,  use  of,  400 
Antipyrin,  use  of,  764 
Antiseptic   powders,   antiseptic  washes 

and,  use  of,  439,  679,  738,  791 
Antitoxin,  formation  of,  57 

streptococcus,  use  of,  150 
Antrum,  empyema  of,  626 
Aphtha,  769 

Aqua  regia,  use  of,  536,  549 
Aristol,  use  of,  429 
Arsenic,  accidents  with,  528 

action  of,  on  gum  tissue,  528 
on  pulp  tissue,  521 
variations  in,  513 

apical  hyperemia  from,  521 

coverings  for,  527 

formulae  for,  525 

iodide  of,  use  of,  488 

mummifying  paste  and,  530 

necrosis  from,  529 

objections  to,  524 

pocket  for,  528 

pulp  hyperemia  from,  521 

in  pulp  nodule,  464 

resistance  to,  464,  492,  524 

second  application  of,  524,  528 

suffusion  from,  522,  524,  531 

use  of,  492,  525 

danger  of,  492,  528,  645 
Arsenical  fiber,  526 
Asperin,  use  of,  491 
Astringents,  use  of,  126,  679,  738 
Atomizer,  use  of,  739 
Atrophy,  79,  253 

marginal,  of  gum,  690 

Harlan's  method  in,  690 
Atropin,  use  of,  381,  649 
Attachment  of  teeth,  265,  266 
Auto-intoxication,  general  malnutrition 
as  cause  of,  93 

oral,  effects  of,  684 


B 


Bacteria,  action  of  gastric  juice  upon, 
54 
aerogenic,  45 
in  blood,  44,  49 
as  cause  of  disease,  36 

of  inflammation,  131 
chemical  composition  of,  39 
chromogenic,  45 


Bacteria,  classification  of,  41 

conditions  antagonizing,  53 

of  dental  caries,  340,  342,  343, 
362,  378,  633 

destruction  of,  by  tissue,  53 

division  of,  in  blood,  45 

effect  of  blood  reaction  upon,  64 

external  antagonistic  agencies,  65 

facultative,  45 

fermenting  action  of,  45 

ferments  of,  46,  47 

forms  of,  41 

immunity  to,  56,  57,  61 

intoxication  and  general  infection 
by,  44,  48,  49,  53,  55,  136,  146, 
148,  234,  439,  603,  631,  742,  781 

life  of,  conditions  of,  40,  45 

localization  of,  44 

media  of,  40 

motility  of,  40 

of  mouth,  50 

obligate,  45 

parasitic,  44 

pathogenic,  49,  51 

penetration  of  root  tubules  by,  640" 
of  secondary  dentin  by,  457, 
498 

photogenic,  45 

plaques  of,  348,  362 

position  in  vegetable  kingdom,  36 

predisposition  to,  action  of,  30,  31, 
50 

products  of,  48 

pyogenic,  132 

resistance  to,  53 

saprophytic,  45 

spore  formation  of,  43 

spreading  of,  in  tissue,  49 

zooglea  of,  43 

zymogenic,  45 
Bacterial  plaques  in  dental  caries,  340, 

362 
Balsam  of  Peru,  use  of,  622,  624,  634, 

738 
Band,  dental,  159 
Bandage,  use  of,  126 
Beck's  bismuth  paste,  622,  624,  625,  739 
Benzoic  acid,  use  of,  679 
Benzoin,  use  of,  476,  482,  490 
Bilein,  use  of,  689 

Bismuth,  subnitrate,  use  of,  207,  739 
Black,  glands  of,  165,  193 
Black's  1-2-3  mixture,  use  of,  739 

operation  for  scar,  630 
Blastomycosis,  39,  769 
Bleaching  agents,  use  of,  581 
Blindness,  dental,  cause  of,  762 
Blisters,  use  of,  125 
Blood,  alterations  in,  113 

bacteria  in,  44-49 

coagulation  of,  116 

extravasation  of,  119,  126,  480,  484, 
507 

pressure,  123 


INDEX 


795 


Blood,    reaction      of,     as    immunizing 
factor,  64 
supply  to  teeth  and  jaws,  190 
Bloodletting  in  inflammation,  etc.,  138, 

236  491 
Blue  light,  use  of,  400,  599,  642 
Bodkin,  wire,  use  of,  442 
Bone,  caries  of,  89,  144,  617,  635 
of  face,  embryology  of,  153 
infection   of,   from   dental   lesions, 

633,  635 
inflammation  of,  142,  633 
of  jaw,  crypts  of,  166 

development  of,  165 
necrosis  of,  145 

from  alveolodental  abscess,  633 
from  syphilis,  595,  780 
perforation  of,  in  abscess,  601,  614 
regeneration  of,  146 
resorption  of,  146,  687 

in  gingivitis,  690,  701 
septa,  166 
Borax.     See  Sodium  biborate. 
Boric  acid,  use  of,  764 
Boroglycerin,  use  of,  680 
Brewer's  yeast,  use  of,  137 
Broaches,  Downie,  use  of,  534 
Swiss,  554 
use  of,  534,  554 
Bromural,  use  of,  400 
Brush,  use  of,  439 
Bruxomania,  301 


Caffein,  use  of,  605,  764 
Calcareous  infiltration,  87 
Calcific  degeneration  of  pulp,  466 
Calcification  of  teeth,  161 

tubular,  449 
Calcium  chloride,  use  of,  121 
lactate,  use  of,  121 
salts  in  blood,  696 
in  pus,  711 
Calcoglobulin,  161,  164,  454,  462 
Calcospherites,  chemical  composition  of, 
161 
in  dentin,  180 
in  enamel,  176 
in  pulp  nodule,  460 
Calculi,  basis  of,  88,  693 
Calculus,  analysis  of,  694 
hematogenic,  711 
origin  of,  693 
pyogenic,  711 
salivary,  692 

analysis  of,  694 
foreign  bodies  in,  695 
hardening  of,  699  • 
hematogenic,  711 
•  mode  of  deposit  of,  698 
occurrence  of,  693 
organic  factor  of,  697 


Calculus,  salivary,  origin  of,  693 

pathological  effects  of,  701 
pyogenic,  711 
removal  of,  704 
scalers  for,  702,  703,  704 
structure  of,  695 
treatment  of,  704 
varieties  of,  692 
sanguinary,  711 
subgingival,  708 
Calendula,  use  of,  680 
Callahan  method,  536 
Calomel,  use  of,  321,  776 
Campho-phenique.  See  Phenol  camphor. 
Canada  balsam,  use  of,  423,  553 
Canals,  accidents  in  opening,  548 
continuity  of,  lost,  432 
fillings,  removal  of,  575,  641 
imperfectly  filled,  results  of,  641 
root,  enlargement  of,  533 
topography  of,  541-543 
Cancrum  oris,  772 
Cantharides,  use  of,  532 
Cantilever  wire  spur,  use  of,  678 
Capping  for  pulp,  427 
Capsicum  plaster,  use  of,  476 
Carbohydrates  in  dental  caries,  340,  344, 

347 
Carbolic  acid,  use  of,  207,  235,  401,  411, 
412,  414,  418,  475,  490,  496,  520,  531, 
601,  739,  619 
Carbon  dioxid,  defective  elimination  of, 
96,  316 
paper,  use  of,  666 
Carcinoma,  78,  784 
Caries  of  bone,  89,  144,  617,  635 
dental,  337 

acids  in,  343 

neutralization  of,  376,  415, 
443 
age  in,  357 
alkalies  in,  443 
arrangement  of  teeth  in,  351 
bacteria  of,  342,  344,  364,  369, 

378 
bacterial  plaque  in,  348,  362 
bodily  condition  in,  358 
calcareous  waters  in,  357 
causes  of,  340,  344,  347 

bacterial,  340,  342,  344 
exciting,  339 

synopsis  of,  340 
predisposing,  local,  349 
systemic,  356 
in  cementum,  384 
chemical  reactions  in,  344,  376 
clinical  history  of,  385 
deep-seated,  416,  418 
defects  of  fillings  in,  351,  379 
dentin  in,  371 

decalcification  of,  372 
secondary,  382,  388 
diagnosis  of,  390 
diet  in,  346,  352,  361,  445 


796 


INDEX 


Caries,  dental,  eburnation  in,  383 

effect  of  malnutrition  upon,  96 

in  enamel,  362,  340 

experiments  in,  341 

ferments  in,  341,  375,  377,  379 

filth  as  a  protection  from,  349, 
361 

foodstuffs  in,  346 

glycogenic,  346,  355,  358,  360 

heredity  in,  356 

history  of,  337 
clinical,  385 

inception  of,  340,  362,  385 
location  of,  362 

lactates  formed  in,  343,  376 

lactic  acid  in,  343 

liquefaction  foci  in,  378 

loss  of  crown  by,  431 
of  root  by,  431 
of  tissues  in,  380 

Miller's    general    experiments 
on,  341 

morbid  anatomy  of,  362 

mucin  in,  355 

of  Nasmyth's  membrane,  371 

pathology  of,  362 

penetrating,  387 

perforation  by,  389,  428 

periodicity  in,  357 

pigmentation  in,  383 

prenatal  influence  in,  356 

prognosis  of,  392 

progress  of,  386 

saliva  in,  354,  443 

prophylaxis  of,  437 

pulp  in,  almost  exposed,  421 
exposed,  425 

recurrence  of,  436 

relative  liability  of  teeth  to,  385 

saliva  in,  354,  443 

school  children  and,  357,  358, 
438 

of  secondary  dentin,  382-388 

self -healed,  371 

simple,  416,  417 

spreading,  387 

stages  of,  396 

structure  of  teeth  in,  352,  388 

sulphocyanate  in,  359,  360 

superficial,  416 

symptoms  of,  390 

of  temporary  teeth,  432 

terminations  of,  388 

therapeutics  of,  416 

toxic  effects  of,  438 

transparent  zone  in,  380,  387 

tube  casts  in,  380 

under  fillings  in,  379 
Caroid,  use  of,  137 
Caseation,  83 

Castor  oil,  use  of,  207,  634,  764 
Catabolism,  23 

Cataphoresis  in  hypersensitive  dentin, 
403,  419 


Cataphoresis,  use  of,  520 

Cataplasma  kaolini,   use   of,   237,   600, 

605 
Cathartics,  use  of,  125,  600 
Caush,  tubes  of,  in  enamel,  174 
Caustics,  use  of,  137 
Cautery,  actual,  use  of,  311,  415 

•     electric,  use  of,  311,  415 
Cavitine,  use  of,  418,  419,  423 
Cells,  chemical  changes  in,  23,  24 
composition  of,  17 
giant,  67,  218 
hypertrophy  of,  67 
life  conditions  of,  25 
movements  of,  18 
nucleus  of,  18 
properties  of,  19 

phagocytic,  19 
receptors  of,  24,  59 
reproduction  of,  20 
stimulation  of,  effects  of,  20,  21,  66 
stimuli  of,  20 
Cellulitis,  submaxillary,  787 
Cement  substance,  162,  163,  167 
solution  of,  363,  368 
oxychlorid  of  zinc.    See  Zinc, 
oxyphosphate  of  copper.    See  Cop- 
per, 
oxysulphate  of  zinc.    See  Zinc, 
sihcate,  use  of,  322,  418 
zinc  phosphate.    See  Zinc. 
Cementum  in  dental  caries,  384,  417 
formation  of,  167 
histology  of,  167,  182 
malformations  of,  microscopic,  250 
nutritional  relation  to  dentin,  183 
relation  of,  to  enamel,  174,  182 
repair  of,  324 
Chalk  mixture,  use  of,  207 

use  of,  414,  442 
Chancre  of  hands,  789 

of  mouth,  777 
Cheek,  distention  of,  by  air  pressure, 
576,  621 
swelling  of,  605 
Chemotaxis,  55 
Chewing  gum,  use  of,  444 
Chloroform,  use  of,  234,  418,  476,  482, 

551 
Chloro-percha,    use    of,  398,   414,   476, 

482,  575 
Chlorophyll,  chemical  action  of,  39 
Chlorosis,  115 
Chorea  from  dental  disease,  653 

from  dentition,  232 
Chromogenic  bacteria,  45 
Cinchona,  use  of,  738 
Cinnamon,  oil  of,  use  of,  739 
Circulation,  disturbances  of,  113 

local,  122 
Cleansing  of  teeth,  439,  705 
Cleft  palate,  embryology  of,  156 
Clot,  absorption  of,  142 
healing  under,  142 


INDEX 


797 


Clot,  septic,  119,  151 

Cloudy  swelling,  83 

Cloves,  oil  of,  use  of,  401,  414,  427,  475 

Coagulants,  use  of,  121,  410,  526 

Coagulation  of  blood,  116,  130,  132 

necrosis,  90,  132 
Cobalt,  use  of,  526 
Cocain,  systemic  effects  of,  519 

use  of,  403,  411,  475,  515,  634 
Codein,  use  of,  491 
Cold,  use  of,  124,  138,  204,  236 
Colloid  degeneration,  86,  511 
Coloboma,  81 

Colophony,  use  of,  414,  553 
Color  of  teeth,  299,  329,  580 
Complement,  61 
Compress,  use  of,  120,  126,  606 
Concrescence  of  teeth,  263 
diagnosis  of,  233 
Conical  teeth,  253 
Constipation,  dental  pain  from,  763 
Copper  amalgam,  use  of,  430,  438,  507 

oxyphosphate  of,  use  of,  415,  507 

sulphate,  use  of,  738,  781 
Cords,  dental,  159,  170 
Cotton  root  dressings,  554,  574,  621 

salicylized,  use' of,  725 

tampons,  danger  of,  604,  633 
Counterirritants,  use  of,  145,  476 
Counterpressure  in  opening  tooth,  598 
Crede's  ointment,  use  of,  150 
Creosote,  use  of,  552 
Cresol,  use  of.    See  Formocresol. 
Crowns,  cantilever,  use  of,  430 

loss  of,  by  caries,  431 

removable,  584 

use  of,  431 
Crypts  of  teeth,  relations  of,  166,  170, 

175 
Cup  gum,  use  of,  621 
Cups,  use  of,  125 
Curette,  use  of,  137 
Cusps,  supplemental,  270 
Cycle,  vicious,  30 

Cysts,  associated  with  apical  conditions, 
614,  642 

causes  of,  68 

dentigerous,  69,  283 

dermoid,  69 

teeth  in,  70 

impacted  teeth  as  cause  of,  68,  283 

varieties  of,  68 


Deafness,  dental,  cause  of,  653,  762 
Decalcification  of  dentin  in  dental  caries, 
372 

of  teeth,  66,  217 
Degeneration,  81 

calcific,  of  pulp,  466 

cloudy,  of  pulp,  511 

colloid,  86 


Degeneration,  colloid,  of  pulp,  511 
fatty,  81 

of  pulp,  511 
fibroid,  507,  669 
of  pericementum,  661,  669 
of  pulp,  507 
hyalin,  85 

in  mouth,  85 

of  mucous  membrane,  85    ' 
lardaceous,  86 
mucoid,  85 

of  mucous  membrane,  85 
of  nerve-end  of  pulp,  514 
of  pericementum,  661 
Dehydrator,  use  of,  401 
Dentifrice,  use  of,  443 
Dentin,  caries  of,  371 

decalcification  in,  371,  422 

secondary,  450 
development  of,  161 
granular  layer  of,  181,  249 
histology  of,  176 
hypersensitivity  of,  181,  393 

causes  of,  393 

diagnosis  of,  390,  393 

pathology  of,  393 

symptoms  of,  396,  753 

treatment  of,  398 
interglobular  spaces  in,  249 
lines  in,  176 

of  Schreger  in,  176,  250 
maKormations      of,      microscopic, 

247 
nutritional  relation  of,  to  cementum, 
183 
to     dentin,     183 
recalcification  of,  424 
repair  of,  324,  450 
resistance  to  acid  by,  660 
resorption  of,  487,  504 
secondary,  182,  424,  450 

bacterial  penetration  of,   457, 
498 
staining  of,  334,  383 

by  putrefaction,  580 
stains  of,  treatment  of,  335,  580 
tubes  of,  176 

tubular  calcification  of,  449 
tumor  of,  453 
Dentinal  fibrils,  162 

papilla,  159 
Dentition,  cause  of,  194 

constitutional     states     modifying, 

200,  214,  231 
normal,  198 
pathological,  198 

as  cause  of  epilepsy,  200 

climate  and  weather  in,  200 

convulsions  in,  203 

diet  in,  208 

first,  198 

headache  in,  203 

hemophilia  in,  206 

hemorrhage  after,  205 


798 


INDEX 


Dentition,  pathological,  intestinal  com- 
plications in,    201, 
207 
feeding  after,  208 
lancing  in,  204 
nervous  disturbances  in,   199, 

202,  213 
paralysis  in,  203 
pulmonary  disturbances  in,  204 
saliva  in,  198 

shock  after  lancing  in,  206 
skin  disorders  in,  204,  206 
strabismus  in,  204 
symptoms  of,  200,  202 
systemic    conditions    influenc- 
ing, 200,  214,  231 
treatment  of,  204 
periods  of,  197 
process  of,  196 
second,  215 

disorders  of,  230 
irregularities  of,  220 
necrosis  in,  231 
pathological,  232 
symptoms  of,  196,  198 
Depletion  of  gum,  491 

of,  pulp,  491 
Derivation,  use  of,  125,  213,  236 
Dermoid  cysts,  69 

teeth  in,  70 
Development  of  face,  153 

of  teeth,  159 
Devitalization  of  pulp,  521 
Devitalizing  fiber,  use  of,  516,  526 
Diabetes  mellitus,  101 
Diagnosis,  definition  of,  26 

forms  of,  26 
Diathesis,  acquired,  94 
gouty,  104 
hemorrhagic,  119 
hyperacid,  93 
Dilaceration  of  teeth,  267 
Discoloration  of  teeth,  329,  580 
Disease,  bacterial  causes  of,  36 
basis  of,  25 
causes  of,  28 
exciting,  28 
predisposing,  30 
clinical  history  of,  26 
existing,  as  a  predisposition,  33 
functional,  25 
predisposition  to,  30 
previous,  as  a  predisposition,  33 
of  teeth,  666 
Dislocation  of  teeth,  671 
Distomolar,  279 
Dobell's  solution,  use  of,  626 
Donaldson  cleaners,  use  of,  534 
Dover's  powders,  use  of,  600 
Downie  broaches,  use  of,  534 
Drill,  Gates-Glidden,  use  of,  537 

spear,  use  of,  598 
Dropsical  infiltration,  86 
Drugs,  intoxication  by,  100,  774 


Dry  cups,  use  of,  125,  621 

socket,  634 
Dryness,  use  of,  401 
Dunn  syringe,  use  of,  738 
Dwarfism  of  teeth,  251 
Dysentery,  ameba  of,  38 


E 


Ear,  disease  of,  from  dental  cause,  653, 

762 
Eburnation  in  dental  caries,  383 
Ecchymosis,  119 

Ehrlich's  theory  of  immunity,  59 
Electrical  disinfection  of  root  canal,  612 
Electricity  in  pulp  putrefaction,  577 

as  test,  564 
Embalming  paste,  use  of,  551 
Emboh,  septic,  119,  151 
Embolism,  118 
Embryology  of  face,  153 

of  teeth,  157 
Emetin,  use  of,  739 
Emphysema  of  cheek  from  air  pressure, 

576,  621 
Empyema  of  antrum,  626 
Enamel,  agenesia  of,  260 

in  dental  caries,  340,  362 

development  of,  162 

formation  of,  effect  of  exanthemata 
upon,  253 

fracture  of,  322 

histology  of,  172 

hypoplasia  of,  253 

imbrications  of,  245 

hues  of  Schreger  in,  174 

maKormation  of,  macroscopic,  251 
microscopic,  239 

nodule,  268 

opaque  spots  in,  240 

organ,  development  of,  159 

organic  matter  in,  172,  242 

parts  of,  172 

relation  of,  to  cementum,  174 

resorption  of,  312 

rod,  163 

sensitivity  of,  396 

stains  upon,  331 

striae  of,  163,  244 

stripes  of  Retzius  in,  174,  244 
of  Schreger  in,  174,  245 

tubes  of,  173 

Caush's,  173 

unusual  location  of,  268 
Encystment  of  teeth,  283 
Endarteritis  obliterans,  77,  688 
Energy,  nerve,  loss  of,  110 

sources  of,  23,  99 
Epilepsy  from  dental  disease,  200,  653 

pathological  dentition  as  cause  of, 
200 
Epizootic  stomatitis,  712 
Equinia,  772 


INDEX 


799 


Ergot,  use  of,  121,  124 
Erosion  of  teeth,  313 
acids  in,  314 

extraneous,  317 
effects  of,  319 

malnutrition  upon,  96,  316 
possible  action  of  glycogen  in, 

84 
treatment  of,  321 
Eruption  of  teeth,  causes  of.    See  Den- 
tition. 
Escharotics,  effects  of,  29,  645 
Ether,  use  of,  398,  402,  519 
Ethyl  chlorid,  use  of,  402 
Etiology,  definition  of,  26,  28 
Eucalyptol,  use  of,  551,  575 
Euca-percha,  use  of,  551,  639 
Eugenol,  use  of,  423,  475,  476 
Evans'  root  drier,  use  of,  531,  553 
Exanthemata,  152 

malformations  caused  by,  152,  253 
necrosis  caused  by,  152,  214,  231 
Excess  of  teeth,  278 
Exostosis  of  alveolar  process,  653 
Extirpation  of  pulp,  532 
Extravasation  of  blood.    See  Blood. 
Eye,  disease  of,  from  dental  cause,  653, 
758,  758 


Face,  development  of,  153 

embryology  of,  153 

fistula  on,  treatment  of,  606,  630 
Farradism  as  test,  564 
Fat,  degeneration  of,  81 

infiltration  of,  81 

necrosis  of,  91 
Fermentation,  bacteria  as  causes  of,  45 

definition  of,  45 

products  of,  46 

of  proteid  matter,  47 
Ferments,  organized,  46 

unorganized,  46 

varieties  of,  47 
Fever,  146 

Fevers,  eruption,  773 
Fibrin,  formation  of,  116 
Fibroma,  74 

Fibrosis.    See  Degeneration. 
Filling  material,  use  of,  309,  321,  416, 

426,  4.38 
Fillings,  combination  of,  422 
Fistulse,  134 

in  antrum,  626 

causes  of,  617 

on  face,  threatened,  606,  630 
treatment  of,  630 

heahng  of,  622 

making  artificial,  601,  614 

non-healing  of,  621 

packing,  623 

premature  closure  of,  137,  604 
Flagg's  operation  for  scar,  628 


Fletcher's  carbolized  resin,  use  of,  414, 

429 
Flexion  of  teeth,  267 
Floss  silk,  use  of,  391,  441 
Follicle,  dental,  167,  170 
wall  of,  161,  168 

becomes  pericementum,  168 
Food,  chemical  changes  in,  24 
concentrated,  use  of,  150 
supply,  abnormal,  28,  94 
Formaldehyd,  action  of,  upon  products 
of  putrefaction,  572 
uses  of,  413,  477,  496,  501,  517,  544, 
546,  680,  790 
Formocresol,  use  of,  496,  546,  612,  639, 

640 
Formo-percha,  use  of,  551,  578,  612,  621 
Fracture  of  alveolar  process,  671 
of  teeth,  322,  571 

repair  of,  324,  451 
reunited,  324 
treatment  of,  326 
Fungi,  animal,  36 
as  ferments,  45 
vegetable,  36 
Fungous  gum,  429 
Fusion  of  teeth,  261 


G 


Gall-stones,  origin  of,  81,  693 
Galvanism,  sterilization  by,  612 

as  test,  564 
Gangrene,  89,  91 

circumscribed,  92 
dry,  91 
moist,  91 

discoloration  from,  580 
of  pulp,  562 
dry,  562 
moist,  565 
partial,  570,  580 
Gastric  juice,  action  of,  on  bacteria,  49 
Gaultheria,  oil  of,  use  of,  739 
Gelatin,  use  and  danger  of,  120 
Gemination  of  teeth,  266 
Geranium-formol,  use  of,  572 
Germicides,  action  of,  65,  791 
Giantism  of  teeth,  251 
Gingivitis,  673 

antiseptic  washes  in,  679 
astringent  washes  in,  679 
deeply  seated,  682 

interstitial,  682 
marginal,  674 

resorption  of  bone  in,  687,  701 
systemic  causes  of,  683 
Glanders,  772 
Glands,  pericemental,  165 
Glycerin,  use  of,  237,  402 
Glycogen  in  caries,  346,  355,  358,  359. 
360 
infiltration  of,   84,   355 


800 


INDEX 


Glycogenic  infiltration  in  dental  caries, 

355 
Gonorrhea  of  mouth,  781 
Gout,  103 

chronic,  103 

contrasted  with  rheumatism,  108 

diet  in,  105 

oral  effects  of,  747 

relation  of,  to  teeth,  710 

salts  deposited  in,  103 

treatment  of,  105 
Goutiness,  104 

treatment  of,  105 
Granulations  in  regeneration,  138,  146 
Greenfield's  artificial  root,  625 
Grippe.    See  La  Grippe. 
Guards,  use  of,  477,  599 
Guillotine,  gum,  235 
Gum,  depletion  of,  491,  604 

glycogenic  infiltration  of,  84 

hyperplastic,  389,  429,  506 

laceration  of,  671 

lancing  of,  204,  235,  604 

marginal  atrophy  of,  690 
Harlan's  method  in,  690 

tissue,  action  of  arsenic  on,  528 
Gutta-percha,    eucalyptol    solution    of, 
use  of,  551,  639 

use  of,  418,  421,  423,  430,  433,  476, 
507,  550,  638 


H 


Hair,  teeth  and,  70,  276 
Halisteresis  ossium,  146,  687 
Hamamelis  distillate,  use  of,  604 
Hands,  sterilization  of,  790 
Hare-lip,  157 

Harlan's  method  in  atrophy,  690 
Headache  in  dentition,  203 

from  impaction,  294 

from  pulp  diseases,  756 
HeaHng  by  second  intention,  140 

under  a  clot  or  scab,  142 
Heat,  use  of,  137,  606 
Hematogenic  calculus,  711 
Hemoglobin,  derivatives  of,  89,  580 
Hemophilia,  119 

in  dentition,  206 
Hemorrhage,  acetanihd  as  cause  of,  120 

after  extraction,  672 
pulp  removal,  518 

replantation  for,  121 

treatment  of,  120 

varieties  of,  119 
Hemorrhagic  diathesis,  119 

sex  in,  120 
Heredity  as  a  predisposition,  33 
Herpes  labialis,  783 

zoster,  783 
Hertwig  root,  sheath  of,  165 
Heteroplasty    following    amputation    of 
natural  roots,  728 


High-frequency  current,  563,  623,  739 
Histology,  morbid,  25 
Hoffendahl,  electric  method  of,  577 
Hot  water,  use  of,  410 
Howship's  lacunae,  146,  658 
Hutchinson's  teeth,  254 
Hydrastis,  use  of,  121 
Hydrogen   dioxid,   208,   235,   496,   582, 
623,  706,  770 
dangers  of,  614 
Hydronaphthol,  use  of,  623,  691 
Hygiene,  definition  of,  27 
Hyoscyamin,  use  of,  400 
Hyperacidity.    See  Acidity. 
Hyperacidosis,  93 
Hypercementosis,  650 

reflex  neuroses  from,  653 
Hyperemia,  arterial,  122 
collateral,  123 
compensatory,  123 
degrees  of,  124 
pathology  of,  125 
of  pulp,  468 

arterial,  468 

devitalization  in,  478 

from  arsenic,  521 

from  electric  action,  479 

from  hypercementosis,  653 

idiopathic,  471,  478 

thermal  toleration  in,  474,  478 

venous,  479 

devitalization  in,  524 
from  hanging,  482 
reflex,  123 
as  a  resistance  to  infection,  124 
results  of,  123 
symptoms  of,  124,  471,  482 
treatment  of,  124 
venous,  125 

suffusion  from,  480 
Hypernutrition,  66 
Hyperplasia,  68,  503,  506 
of  gum,  389 
of  pulp,  389 
Hypersensitivity    of    dentin,    393.     See 

Dentin. 
Hypertrophy  of  cells,  67 
Hypnotism,  use  of,  400 
Hyponutrition,  79 
Hypophosphites,  use  of,  488 
Hypoplasia,  79,  253 
of  enamel,  253 
Hysteria,  233 


IcHTHYOL,  use  of,  773 
Immunity,  34,  56 

acquired,  57 

blood  reaction  in,  64 

Ehrlich's  theory  of,  59 

lost,  35,  56 

natural,  56 
Impaction  of  teeth,  283  , 


INDEX 


801 


Impaction  of  teeth,  as  cause  of  cysts, 
69,  294 
death  of  pulp  from,  293 
diagnosis  of,  295 
headache  from,  294 
neuralgia  from,  292 
resorption  of  roots  from,  285, 

295,  657 
symptoms  of,  292 
treatment  of,  296 
Implantation,  625 
Inanition,  99 
Indican  as  an   index  for  malnutrition, 

100,  685 
Indol,  100 

Infants,  feeding  of,  208 
Infarction,  119 

of  pulp,  507 
Infection,  classes  of,  49 
general  septic,  149 
of  mouth,  766 

predisposition  to,  30,  31,  56 
resistance  of  tissue  to,  52 
spreading  of,  48 
Infiltration,  calcareous,  87 
dropsical,  86 
fatty,  81 

glycogenic,  74,  355 
pigmentary,  88 
Inflammation,  127 

bacteria  in,  127,  131 
bloodletting  in,  138 
of  bone,  143 
catarrhal,  130 
causes  of,  127 
coagulation  in,  129,  132 
derivation  in,  138 
exudates  of,  126 
infective,  131 
necrosis  in,  132 
pathology  of,  127,  131 
of  pulp,  483 

chi'onic,  501 
resolution  in,  132 
simple,  127 
stimulation  in,  138 
suppurative,  132 
symptoms  of,  131,  135 

general,  131,  135,  136 
treatment  of,  137 
Injury  of  teeth,  322 
Inoculation  by  bacteria,  49 
Insanity  from  dental  disease,  294,  759 
Insomnia  from  dental  disease,  439,  762 
Instruments,  sterilization  of,  790 
Insulator,  311 

Intermaxillary  bone,  failure  of  develop- 
ment of,  168 
formation  of,  153 
Intestinal  complications  in  pathological 

dentition,  201,  297 
Intoxications,  100 
acid,  102 

bacterial,  101,  148 
51 


Intoxications,  drug,  100 

intestinal,  94,  688 

intrinsic,  101,  102 

septic,  148 
Intubation  of  root,  584 
Involucrum,  145 
lodin,  dental,  tincture  of,  476 

use  of,  235,  412,  476,  507,  530,  549, 
572,  579,  770,  792 
Iodoform,  use  of,  549,  623 
lodoglycerol,  use  of,  738 
Iron,  chloride  of,  tincture  of,  use  of, 
353,  605 

dialyzed,  use  of,  530 
Ischemia,  122 


Jaw,  development  of,  153 

growth  of,  cause  of,  172 
Jodoformagen,  use  of,  423,  427 
Joining  of  teeth,  421,  699 
Jugulation  of  pulp,  481 


Kalium  natrium,  use  of,  536,  577 
Karyokinesis,  20 
Kerr  broaches,  uses  of,  534 
Kowarska's  paste,  729 
Krameria,  use  of,  680 


Laceration  of  soft  tissues,  672 

Lactic  acid,  use  of,  738 

Lacunae,  Howship's,  146 

La  grippe,  as  cause  of  reflex  pain,  763 

Lanohn,  use  of,  149,  776 

Laudanum,  use  of,  121,  672 

Lead,  oral  effects  of,  649 

water,  use  of,  121 
Leeches,  use  of,  600 
Leprosy,  786 
Leukemia,  115 
Leukocytosis,  115 
Leukoplakia  buccahs,  783 
Lichen  planus,  784 
Light,  electric,  use  of,  391 
Lime-water,  use  of,  446 
Linings,  use  of,  419 
Listeririe,  use  of,  207,  770,  790 
Lithemia,  106 

Litliia  salts,  use  of,  689,  741 
Liver,  functions  of,  98 

in  general  malnutrition,  95,  98 
Ludwig's  angina,  235,  787 
Lupus  of  mouth,  780 
Luxation  of  teeth,  639 
Lymphangitis,  605 


802 


INDEX 


M 


Magnesia,  milk  of,  use  of,  321,  415 

sulphate  of,  use  of,  125,  600,  697 
Malaria,  dental  pain  from,  763 
Malformations,  macroscopic,  251 
microscopic,  239 
of  roots,  271,  545 
of  teeth,  239 
Malnutrition,  causes  of,  23,  93 
from  gingivitis,  742 
general,  93.      See  Bacteria  intoxi- 
cations, 
auto-intoxication  in,  93 
diet  in,  97,  105 
Malocclusion  of  teeth,  664 
causes  of,  219 
classification  of,  223 
Malpositions  of  teeth,  281 
Massage,  use  of,  605,  738 

vibratory,  605 
Maxillae,  embryology  of,  154 
Maxillary  rampart,  159 
Mechanical  injury  of  teeth,  322 

union  of  teeth,  266 
Meckel's  cartilage,  158 
Melancholia  from  dental  disease,  762 
Menthol,  use  of,  401,  482,  496,  540,  764 
Menthol-phenol,  use  of,  475,  648 
Mercury,  bichlorid  of,  use  of,  150,  235, 
559,  605,  621,  624,  648,  649,  681, 
789,  792 
as  cause  of  stomatitis,  648 
oral  effects  of,  232,  648,  681 
Talbot's  experiments  on  dogs  with, 
644 
Metabohsm,  diseases  of,  24,  93 
Metastasis,  56,  144 
Methyl  chlorid,  use  of,  402 
Microorganisms,  as  disease  causes,  36 
Milk,  modified,  208 
Mitosis,  20 

Morphin,  use  of,  138,  399,  491,  600 
Motor  reflexes  from  dental  disease,  761 
Mouth,  actinomycosis  of,  780 
asepsis  of,  788 
bacteria  of,  50 

pathogenic,  51 
breathing,  224 
development  of,  153 
gangrene  of,  772 
gonorrhea  of,  781 
hyaline  degeneration  in,  85 
infections  of,  766 
inflammation  of.    See  Stomatitis, 
lamp,  electric,  use  of,  390,  626 
sepsis  from.     See  Bacteria  intoxi- 
cation, 
soft  tissues  of,  laceration  of,  672 
sterilization  of,  788 
syphilis  of,  775 
tuberculosis  of,  780 
washes,  application  of,  679,  788 
Mucin,  characteristics  of,  85 


Mucin  in  dental  caries,  355 
Mucoid  degeneration,  85 

of  mucous  membrane,  85 
Mucous  membrane,  glycogen  in,  84 
hyaline  degeneration  of,  85 
mucoid  degeneration  of,  85 
overstimulation  of,   effects  of, 
84 
Mummification  of  pulp,  556,  558 
Mummifying  paste,  arsenic  and,  530 
Mustard,  use  of,  125,  789 
Myers'  syringe,  use  of,  406,  518 
Myrrh,  tincture  of,  use  of,  649,  681 


N 


Nasmyth's  membrane,  165,  172 

in  dental  caries,  371 
Necrobiosis,  89 
Necrosis,  89 

after  extraction,  634 

of  alveolar  bone,  608 

of  bone,  145 

arsenical,  529 

from  alveolodental  abscess,  635 

from  syphilis,  636,  775 

coagulation,  90,  132 

etiology  of,  89 

of  fat,  91 

from  exanthemata,  231 

from  mercury,  232,  648 

from  typhoid  fever,  221 

liquefaction  in,  91 

phosphorus  and,  785 

varieties  of,  89 
Neoplasm  of  pulp,  511 
Nerve  energy,  loss  of,  110 

fifth,  754 

sensory,  of  face,  754 

supply,  abnormal,  29 

trophic  influence  of,  29 

vasomotor,  122,  29 
Nervocidin,  use  of,  520 
Nervous  disturbances  in  dental  disease, 
203  752 
in  dentition,  193,  204 
Neuman,  sheath  of,  162,  176 
Neuralgia,  cause  of,  270,  389 

from  hypercementosis,  653 

from  hypersensitive  dentin,  753 

from  impacted  teeth,  277 

from  pericemental  disease,  757 

from  pulp  disease,  755 

from  secondary  dentin,  433 

treatment  of,  764 
Neurasthenia,  110 
Neuroma,  155 
Neuroses,  reflex,  752 
Nitric  acid,  use  of,  311   ■ 
Nitrous  oxid  gas,  use  of,  398,  491 
Nodule,  cemental,  273 

in  pulp,  458 
Noma,  235,  772 


INDEX 


803 


Non-conductors,  uses  of,  419 
Novocain,  use  of,  407,  518 
Number  of  teeth,  variations  in,  275 
Nutrition,  basis  of,  22 

deficiency  of,  79 

disturbances  of,  24,  28,  30,  66,  93 

excess  of,  66 


Obligate  bacteria,  45 
Odontalgia,  phantom,  759 
Odontoblasts,  160,  178 

atrophy  of,  453,  510 

relation  of,  to  sensory  nerves,  181 
Odontomata,  273 
Oligocythemia,  107 
Opium,  use  of,  121,  125,  207,  234,  602 
Opsonic  index,  raising  of,  622,  740 
Opsonins,  62 
Organic  matter,  decomposition  of,  45,  47 

fermentation  of,  45 
Organs,  composition  of,  22 
Orthoform,  use  of,  413,  429 
Osteitis,  condensing,  144 

rarefying,  144 
Osteodentin,  456 
Osteomalacia,  146,  446,  687 
Osteomyelitis,  143 
Osteoporosis,  144 
Osteosclerosis,  144 
Overarch  bar,  use  of,  664 
Overfeeding,  99 
Overuse  of  teeth,  661,  664 
Oxalm-ia,  110 
Oxidation,  deficiency  of,  93 

excessive,  93 
Oxygen,  nascent,  use  of,  582 


Pain,  dental,  from  other  sources  than 
dental,  763 

postextraction,  603,  633,  672 
Palate,  cleft,  cause  of,  156 
Papain,  use  of,  560 
Papoid,  use  of,  137 
Paraffin,  use  of,  552,  739 
Paraform,  use  of,  612 
Paraglossus,  311 
Paralysis  from  dental  disease,  760 

in  dentition,  203 
Paramolar,  279 
Parasitic  bacteria,  44 
Pathogenesis,  definition  of,  26 
Pathogenic  bacteria,  44,  49 
Pathology,  basis  of,  17,  25 

dental,  definition  of,  17 

general,  definition  of,  17 
Pediluvium,  hot,  use  of,  118,  600 
Peptones,  47,  126  _ 
Perforation  by  accident,  548 

by  caries,  389,  428 


Perforation  as  cause  of  abscess  of  root, 
619 

filling  of,  561 

in  septic  cases,  637 
Pericemental  abscess,  745 
Pericementitis,  585.    See  also  Pyorrhea 
alveolaris. 

acute,  septic,  apical,  581 
extraction  in,  602 

beginning  at  gum  margin,  674 

chi'onic,  septic,  apical,  609 

classification  of,  585 

gouty,  710 

non-pm-ulent,  639 

non-septic,  644 
chemical,  645 
results  of,  650 
symptomatic,  648 

phagedenic,  676 

septic  at  bifurcations  of  roots,  643 

symptomatology  of,  585 

traumatic,  644 
Pericementum,  blood  supply  to,  190 

calcospherites  in,  193 

cellular  element  of,  186,  193 

degeneration  of,  661 
fibroid,  669 

development  of,  168 

diseases  of,  586 

fibrosis  of,  669 

function  of,  184 

glands  of,  1^5,  193 

histology  of,  184 

nerves  of,  190 

overuse  of,  661 
Periostitis,  143 

maxillary,  617 

proliferative,  143 

suppurative,  143 
Peru,  balsam  of.    See  Balsam. 
Petechia  119 

Phagocytosis,  19,  55,  152,  622 
Phantom  odontalgia,  759 
Phenacetin,  use  of,  400,  491 
Phenobromate,  use  of,  400 
Phenol  camphor,  use  of,  414,  475,  540, 
672,    689,    739,    771 

sodique,  use  of,  444,  672,  724,  770 
Phenolsulphonic  acid,  619 
Phosphatm-ia,  111 
Phosphor  necrosis,  785 
Phosphorus,  use  of,  81,  785 
Physical  condition,  abnormal,  29 
Physiology,  morbid,  25 
Pigmentary  infiltration,  88 
Pigmentation  in  dental  caries,  383 
Pigments  in  tissue,  88 
Pilocarpin,  oral  effects  of,  648 
Pins,  removal  of,  576 
Piscidia  erythrina,  use  of,  400 
Plantation,  mode  of  attachment  in,  659 

resorption  after,  656 
Plaques,  microbic,  348,  362 
Plaster  of  Paris,  use  of,  427 


804 


INDEX 


Plethora,  113 
Podophyllin,  use  of,  689 
Pointing,  134 
Polycythemia,  113 
Porte-polisher,  use  of,  442 
Potassium  bromid,  use  of,  402 
carbonate,  use  of,  402 
chlorate,  use  of,  206,  444,  649,  681, 

792 
hydrate,  use  of,  411 
permanganate,  use  of, 
sulphocyanate,  use  of,  415 
Poultices,  danger  of,  606 

uses  of,  606 
Powder,  tooth,  use  of,  443 
Precipitins,  62 
Predisposition  to  disease,  30 
general,  30 
local,  33 
Pregnancy,  dental  pain  from,  763 
Pressure  anesthesia,  458,  465,  474,  482, 
496,  516 
hemorrhage  after,  517 
Process,  alveolar,  fracture  of,  672 
Prognosis,  definition  of,  26 
Prophylaxis,  26,  437,  445 
Proteid,  composition  of,  18 
fermentation  of,  47 
use  of,  23 
Protoplasm,  composition  of,  18 

properties  of,  22 
Protozoa  as  disease  causes,  36 
Pseudoodontalgia,  759,  764 
Ptomains,  44,  47 
Pulp,  abscess  of,  497 

action  of  arsenic  on,  521 
anesthesia  of,  405,  415 
blood  supply  of,  178 
capping  of,  426 
cavity,  duphcation  of,  267 

forms  of,  186 
constructive  diseases  of,  449 
death  of,  from  impaction,  294 

symptoms  of,  563 
degeneration  of,  507 
calcific,  465 
cloudy,  486 
colloid,  514 
fatty,  511 
fibroid,  507 
nerve,  514 
depletion  of,  482,  490 
destructive  diseases  of,  468 
devitalization  of,  521 
digestion  of,  560 
exposure  of,  symptoms  of,  425 

treatment  of,  422,  426 
extirpation  of,  532 
gangrene  of,  562 
partial,  570 
histology  of,  176 
hyperemia  of,  468 
arterial,  468 

devitahzation  in,  476 


Pulp,    hyperemia    of,     arterial,     from 
electric  action,  479 
idiopathic,  471,  478 
thermal  toleration  in,  478 
from  arsenic,  521 
venous,  479 

suffusion  in,  480 
hyperplasia  of,  389,  503 
infarction  of,  507 
inflammation  of,  483.    See  Pulpitis, 

chronic,  501 
jugulation  of,  481 
knocking  out,  531 
mummification  of,  556,  558 
neoplasm  of,  511 
nerves  of,  181 
nodules,  458 

arsenic  and,  465 
puncturing  of,  482,  490,  531 
putrefaction  of,  565 
reaction  of,  447 
removal  of,  515 
partial,  557 

special  methods  of,  531 
replantation  of,  vitality  after,  456 
sclerosis  of,  501 
sedation  of,  475 
suppuration  of,  492 
swelling  of,  486 
thermal  tolerance  of,  424 
toughening  of,  538 
ulceration  of,  493 
vitality  of,  tests  for,  563 
Pulpitis,  483 
acute,  484 
chronic,  501 

from  pyorrhea,  666 
hyperplastic,  503 
resorption  of  dentin  in,  487 
Pumice,  use  of,  705 
Pm-pura  hemorrhagica,  786 
Pus    formation,    stages    of,    in    apical 
abscess,589 
varieties  of,  135 
Putrefaction,  47,  565 
formahn  in,  572 
germs  of,  effects  of  electricity  upon, 

577 
of  pulp,  565 
Pyemia,  151,  782 
Pyocyaneo-protein,  use  of,  637 
Pyogenic  calculus,  711 
Pyorrhea  alveolaris,  713 

abscess  secondary  to,  721,  745 
beginning  with  a  marginal  gin- 
givitis, 716 
in  bifurcations  of  roots,  727 
breath  in,  720 

bridge  and  plates  in,  662,  736 
causes  of,  713 

clinical  history  of,  716  , 

dental  caries  and,  687 
diagnosis  of,  716,  723 
!  endarteritis  in,  719 


INDEX 


805 


Pyorrhea  alveolaris,  gum  incision  in,  726 
recession  in,  716 
heteroplasty  of  roots  in,  728 
interstitial   gingivitis   in,    683, 

719 
living  pulps  and,  727 
looseness  in,  719 
malnutritional  factor  in,  740 
not  dependent  upon  calculus, 

743 
opsonic  index  in,  740 
oral  catarrh  in,  720 
pathology  of,  716 
prevention  of  motion  in,  729 
prophylaxis  in,  787,  741 
recurrence  of,  741 
replantation  in,  740 
root  amputation  in,  727 
shifting  of  teeth  in,  665,  720 
splints  for  use  in,  729 
systemic  effects  of,  742 
symptoms  of,  716 
treatment  of,  724 

medicinal  in,  737 
varieties  of,  715 

Pyrozone,  use  of,  531,  582,  624 


QuiNiN,  use  of,  150,  400,  491,  600,  605, 
764 


B 


Rachitis,  110 
Rampart,  maxillary,  159 
Recalcification  of  dentin,  423 
Receptors  of  cells,  24,  59 
Reflex  action,  199,  201,  203,  761 

disorders  of  dental  origin,  752 
of  systemic  origin,  763 

neuroses,  752 

pain,  464,  470,  471 
pathology  of,  752 
Regeneration  of  tissue,  138,  146 
Repair  of  dentin  and  cementum,  324, 

455 
Replantation,     624 

for  hemorrhage,  121 

of  pulp,  vitality  after,  456 

secondary  dentin  after,  456 

of  teeth,  647 
Resorcin,  use  of,  143 
Resorption  of  bone,  146 

varieties  of,  146,  687 

of  enamel,  312 

of  permanent  roots,  655 

of  pulp,  487,  504 

of  temporary  roots,  216 

perforation  by,  219 
Retention  of  teeth,  221 
Retzius,  stripes  of,  in  enamel,  174,  244 


Rhein,  root  methods  of,  539,  540 
Rheumatism,  107 

chronic,  109 

contrasted  with  gout,  108 

muscular,  109 

treatment  of,  108 
Ridge,  dental,  159 
Robinson's  remedy,   use  of,   311,   411, 

415,  418 
Root,  amputation  of,  619,  623,  727 

artificial,  625 

bifurcation,  formation  of,  168 

calcification  of,  167,  171,  176 

canal,  accidents  in  opening,  548 
anatomy  of,  541,  543 
cementum  forming  end  of,  168 
electrical  disinfection  of,  577 
filling  of,  550,  613 
inaccessible  foramina  of,  544 
loss  of  continuity  of,  432 

development  of,  167,  220 

drier,  Evans',  use  of,  531,  552 

filling,  immediate,  539,  576 
removal  of,  549 

fracture  from  putrefaction,  571 

fusion  and  concrescence,  272 

implantation  of,  625 

long  and  short,  270 

loss  of,  by  caries,  389,  432 

malformations  of,  271,  545 

multiple,  271 

perforation,  329 

permanent,  formation  of,  220 
resorption  of,  295,  655 

repair  of,  324 

replantation  of,  647 

resorption  of,  216,  219 
of  permanent,  655 

soap  in,  use  of,  619,  789,  792 

sterilization  of,  571 

systematic  stopping,  613 

temporary,  resorption  of,  216 

transplantation  of,  431,  625 
Rose  geranium,  oil  of,  use  of,  572 
Rubber  band,  use  of,  441 

cup,  use  of,  621,  705 

sore  mouth  and,  771 


S 


Saccharin,  use  of,  207 

SalicyUc  acid,  use  of,  679 

Saliva,  analysis  of,  695 

in  dental  caries,  354,  443 

in  general  malnutrition,  93,  314 

increased  flow  of,  198 

infective  bacteria  in,  50,  781 

lack  of,  354 

relation  of  acid  food  to,  355 

Salivary  calculus,  692.    See  Calculus. 

Salol,  use  of,  150,  207,  553,  605 

Salter,  lines  of,  in  dentin,  176 

Salvarsan,  use  of,  780 


806 


INDEX 


Sandarac,  use  of,  429 

Sanguinary  calculus,  711 

Sapremia,  148 

Saprophytic  bacteria,  45 

Sarcoma,  74 

Scab,  healing  under,  142 

Schizomycetes,  36,  41 

Schreger,  stripes  of,  in  dentin,  176 

in  enamel,  174,  245 
Sclerosis  of  pulp,  501 
Scorbutus,  109,  215,  649,  786 

infantile,  215 

oral  effects  of,  649,  786 
Scurvy.    See  Scorbutus. 
Sedation,  results  of,  21 
Sedatives,  use  of,  475,  482,  490,  501,  648 
Sepsis  dental,  bacterial  intoxication  and, 
439 

general,  of  dental  origin,  439,  631, 
781 

intoxication  from,  bacterial  intoxi- 
cation and,  148,  439 
Septicemia,  149,  235,  782 

from  apical  abscess,  604,  631 
Sequestrum,  89,  92,  145,  785 
Serres,  glands  of,  193 
Serum  therapy,  59,  122 
Sex  as  predisposing  cause  of  disease,  31 
Sheaths  of  Neuman,  162,  176 
Side  chain  theory,  Ehrlich's,  24,  59 
Silicate  cements,  use  of,  322,  418,  424 
Silver,  Crede's  ointment,  use  of,  150 
soluble,  use  of,  150 

nitrate,  use  of,  311,  412,  415,  433, 
438,  477,  530,  624,  770 
Sinus,  134 

Size  of  teeth,  variations  in,  251 
Skin  eruptions,  152,  204,  632 
Slough,  92 

Soap,  use  of,  619,  789,  792 
Sodium  biborate,  use  of,  679,  790 

bicarbonate,  use  of,  412,  423,  490, 
689,  764,  785 

bromid,  use  of,  213 

carbonate,  use  of,  411 

chlorid,  use  of,  412,  549,  681,  689, 
738 

dioxid,  danger  of,  577 

use  of,  336,  412,  549,  576,  582, 
790 

hydrate,  use  of,  411 

potassium  and,  alloy  of,  use  of,  536, 
577 

sulphate,  use  of,  121 
Somnaform,  use  of,  399,  515 
Sphacelus,  87 
Sponge,  use  of,  637 
Stains,  black,  333 

in  dentin,  334 

dyes  and,  333 

green,  331 

metallic,  329 

non-metallic,  331 

red,  333 


Stains,  tobacco,  333 

treatment  of,  334 
Starvation  of  tissue,  99 
Stellate,  reticulum,  160,  164 
Steresol,  use  of,  297 
Sterilization,  dental,  788 
Stimulation,  effects  of,  21,  66 
Staples,  use  of,  328,  421,  643 
Stomatitis,  766 

aphthous,  769,  772 

classification  of  varieties  of,  767 

in  dentition,  204,  206 

epizootic,  772 

follicular,  771 

from  drugs,  774 

from  eruptive  fevers,  773 

from  glanders,  772 

infective  catarrhal,  767 

mercurial,  768 

beneficial  effects  of  mercury  in, 
649,  681 

simple  catarrhal,  767 

symptomatic  catarrhal,  768 

typhoid,  768 

ulcerosa,  677 

ulcerative,  769 
Stopping,  systematic,  613 
Strabismus  in  dentition,  204 
Stratum  intermedium,  160,  165 
Strontium  lactate,  use  of,  121 
Structure  of  teeth,  239,  352,  388 
Strychnin,  use  of,  519,  765 
Subgingival  calculus,  708 
Suffusion,  119,  580 

from  arsenic,  524,  531 

from  hanging,  482 

from  venous  hyperemia,  480 
Sugar  in  diabetes,  101,  360,  358 

as  source  of  energy,  24,  99 
Sulphocyanate,  use  of,  360,  415 
Sulphuric  acid,  use  of,  531,  549,  622, 

624,  738 
Sulphurous  acid,  use  of,  583 
Supernumerary  teeth,  280 
Supplemental  cusps,  270 
Suppuration  in  inflammation,  132 

of  pulp,  492 
Suprarenal  extract,  use  of,  121 
Susceptibility  to  disease,  30 
Symbiosis,  49 
Symptoms,  definition  of,  25 

objective,  26 

subjective,  26 
Synostosis,  dental,  654 
Syphilis,  dental  pain  from,  763 

hereditary,  257 

of  mouth,  775 

necrosis      of      bone      from,     636, 
775 

oral  effects  of,  254 

stigmata  of,  257 
Syphilitic  teeth,  254 
Systematic    stopping    of    troublesome 
root,  613 


INDEX 


807 


Tannin,  use  of,  206,  402 
Tartasol,  use  of,  738 
Temperament,  classes  of,  32 
Therapeutics,  basis  of,  21         > 

definition  of,  17,  26 
Thrombosis,  117,  481,  521 
Thymol,  use  of,  420,  423,  427,  475,  483, 

490,  496,  540 
Thymophen,  use  of,  475 
Tic  douloureux,  464 
Tissue,  composition  of,  23 

excessive  destruction  of,  99 

food  supply  to,  22 

regeneration  of,  138 

resistance  of,  to  bacteria,  53 

starvation  of,  99 

waste,  excessive,  99 
Tomes,  granular  layer  of,  249 
Toxalbumins,  44,  48 
Toxemia,  44,  48,  135,  136,  148 

in  general  malnutrition,  93 
Toxins,  44,  48 

chemotactic  properties  of,  55 

as  ferments,  44 

immunity  to,  57 
Toxoid,  60 
Toxon,  61 
Transparency  of  dental  structures,  382, 

449 
Transparent  zone,  380,  387 
Transplantation,  use  of,  431,  625 
Trephine,  use  of,  328,  643,  602 
Treponema  palhdum,  256 
Trichloracetic  acid,  use  of,  507,  738,  770 
Trigemin,   use  of,   492,   600 
Trioxymethylene,  use  of,  413 
Trophic  disturbance,  29 

from  dental  disease,  763 
Tube  casts  in  dental  caries,  380 
Tuberculosis  of  mouth,  780 
Tubes  of  dentin,  176 

of  enamel,  174 
Tubular  calcification,  449 
Tumors,  72 
Turkish  baths,  use  of,  689,  741 


U 


Ulceration,  92,  136 

of  pulp,  493 
Uremia,  101 


Urates  in  pericementum,  747 

in  tissue,  97 
Uric  acid  in  gout,  103 
Uterine  disease,  dental  pain  from,  763 
Uvula,  bifid,  158 


Vaccine  therapy,  62,  63,  150 

Vapocain,  use  of,  402 

Varnish,  use  of,  419,  421,  423,  476,  477 

Vascular  system,  disturbances  of,  113 

Vasehn,  use  of,  739,  764 

Vasomotor  nerves,  122 

Vegetable  fungi,  36 

Venous  hyperemia,  suffusion  from,  455 

Veratrin,  use  of,  225 

Vibrator,  use  of,  605 

Vincent's  angina,  675,  681 


W 

Wall,  follicular,  161 

Waste,  removal,  abnormal,  28,  94 

Water,  boiling,  as  germicide,  790 

drinking  of,  689,  741 

warm,  use  of,  418 


X-KAYS,  use  of,  612,  623,  739 


Ziehler-Hofpendal,    electric    method 

of,  612 
Zinc  chlorid,  use  of,  410,  484,  517,  621, 
■     679,  738 
iodide,  use  of,  738 
oxid  and  eugenol,  use  of,  423,  427, 
476,  489,  638 
use  of,  427 
oxychlorid  of,  use  of,  411,  415,  423, 

427,  551,  637 
oxyphosphate,    use    of,    232,    419 

421,  423,  476 
oxysulphate,  use  of,  427 
sulphate,  use  of,  427 
sulphocarbolate,  use  of,  738 
Zooglea  of  bacteria,  43 


COLUMBIA   UNIVERSITY 

This  book  is  due  on  the  date  indicated  below,  or  at  the 
expiration  of  a  definite  period  after  the  date  of  borrowing, 
as  provided  by  the  rules  of  the  Library  or  by  special  ar- 
rangement with  the  Librarian  in  charge. 

•DATE  BORROWED 

DATE  DUE 

DATE  BORROWED 

DATE  DUE 

JCT     8  'S8 

OCT  1  5 "3^ 

DEC    61949 

CZe(C38)M50 

COLUMBIA  UNIVERSITY  LIBRARIES  (hsi  stxl 

RK  301  B892  1915  C.1 

A  text-book  of  dental  pathology  and  ther 


2002340801 


RK301  B892 

1915 
Bur chard 
Text-book  of  dental  pathology  and 


